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Module Psy 3 1 1

This module in Physiological Psychology focuses on the anatomy and functions of the central and peripheral nervous systems, including the brain, spinal cord, and neurons. It covers the processes of synapses and neurotransmission, detailing the roles of various brain structures and types of neurons. Students will learn to identify divisions of the nervous system and discuss neurotransmission processes by the end of the module.

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0% found this document useful (0 votes)
22 views44 pages

Module Psy 3 1 1

This module in Physiological Psychology focuses on the anatomy and functions of the central and peripheral nervous systems, including the brain, spinal cord, and neurons. It covers the processes of synapses and neurotransmission, detailing the roles of various brain structures and types of neurons. Students will learn to identify divisions of the nervous system and discuss neurotransmission processes by the end of the module.

Uploaded by

anzuresshanah
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Overview of the Module in Physiological Psychology

This module covers the brain cells, structures, components and chemical interactions that are
involved in order to produce actions.

It also focuses on how the nervous system intertwines with other systems in the body to create a
specific behavior.

Module

1
This module introduces the central nervous system: Anatomy, Structures, Functions, Process of synapses
and neurotransmission.

I. Learning Outcomes:

At the end of the topic, the students should be able to:

1. Identify the anatomical and functional divisions of the nervous system.


2. Discuss the process of synapses and neurotransmission.

II. Topic 1. Anatomy of the Nervous System


1.1 Functions and Structures of the Nervous System
1.2 Cells of Nervous System
1.3 Synapses and Neurotransmission
III. Time Frame: Week 2

IV. Topic Discussion:

Systems and Structures of Nervous System


Divisions of the Nervous System
I. The Central Nervous System

The central nervous system (CNS) controls most functions of the body and mind. It has three components :
the brain, the spinal cord and the neurons (or nerve cells). Each part of the CNS plays an important role in
how the body functions, and the three components of the CNS work together to take in information and how
the body responds

A. Brain
The brain is the center of our thoughts, the interpreter of our external environment, and the origin of control
over body movement. Like a central computer, it interprets information from our eyes (sight), ears (sound),
nose (smell), tongue (taste), and skin (touch), as well as from internal organs such as the stomach.

Main parts of the brain


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The brain has three main parts:

 Cerebrum
 Cerebellum
 Brain stem

The Cerebrum

The cerebrum, the large, outer part of the brain, controls reading, thinking, learning, speech, emotions and
planned muscle movements like walking. It also controls vision, hearing and other senses.

The cerebrum is divided two cerebral hemispheres (halves): left and right. The right half controls the left side
of the body. The left half controls the right side of the body.

Each hemisphere has four sections, called lobes: frontal, parietal, temporal and occipital. Each lobe controls
specific functions. For example, the frontal lobe controls personality, decision-making and reasoning, while
the temporal lobe controls, memory, speech, and sense of smell.

The Cerebellum

The cerebellum, in the back of the brain, controls balance, coordination and fine muscle control (e.g.,
walking). It also functions to maintain posture and equilibrium.

The Brain Stem

The brain stem, at the bottom of the brain, connects the cerebrum with the spinal cord. It includes
the midbrain, the pons, and the medulla. It controls fundamental body functions such as breathing, eye
movements, blood pressure, heartbeat, and swallowing.

Occipital - This is found in the back of the brain. The area is involved with the brain's ability to recognize objects. It is
responsible for our vision.

Temporal lobe - found on either side of the brain and just above the ears. The temporal lobes are responsible for
hearing, memory, meaning, and language. They also play a role in emotion and learning. The temporal lobes are
concerned with interpreting and processing auditory stimuli.

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Parietal lobe - parietal lobes are found behind the frontal lobes, above the temporal lobes, and at the top back of the
brain. They are connected with the processing of nerve impulses related to the senses, such as touch, pain, taste,
pressure, and temperature. They also have language functions.

Frontal lobe - It is concerned with emotions, reasoning, planning, movement, and parts of speech. It is also involved
in purposeful acts such as creativity, judgment, and problem solving, and planning.

Cerebral cortex - cerebral cortex controls your thinking, voluntary movements, language, reasoning, and perception.
In higher mammals the cortex looks like it has lots of wrinkles, grooves and bumps.

Cerebellum - controls your movement, balance, posture, and coordination. New research has also linked it to
thinking, novelty, and emotions.

Limbic system - often referred to as the ‘emotional brain” is found within the cerebellum.

Hypothalamus – controls your body temperature, emotions, hunger, thirst, appetite, digestion and sleep. The
hypothalamus is composed of several different areas and is located at the base of the brain. It is only the size of a pea
(about 1/300 of the total brain weight), but is responsible for some very important behaviors.

Thalamus – controls your sensory integration and motor integration. Receives sensory information and relays it to
the cerebral cortex also sends information to the thalamus which then transmits this information to other parts of
the brain and the brain stem.

Pituitary gland - controls your hormones and it helps to turn food to energy. Without this gland you could eat but
you wouldn't get any energy from the food.

Pineal gland - This part controls your growing and maturing. It is activated by light so if you were born and lived all
your life in a place without a trace of light your pineal gland would never start to work.

Amygdala - The amygdala (there are two of them) control your emotions such as regulating when you're happy or
mad. Your amygdala is very important. Without it you could win the lottery and feel nothing. You wouldn't be happy.

Hippocampas - Forms and stores your memories (scientists think there are other things unknown about the
hippocampas) and is involved in learning. If you didn't have it, you wouldn't be able to remember anything. People
with Alzheimer's disease loose the functioning of their hippocampas.

Mid – brain - this section controls your breathing, reflexes, and your swallowing reflexes. Includes the Thalamus,
Hippocampus, and Amygdala. Every living thing has to have a mid-brain.

Pons - part of the metencephalon in the hindbrain. It is involved in motor control and sensory analysis... for
example, information from the ear first enters the brain in the pons. It has parts that are important for the level of
consciousness and for sleep. Some structures within the pons are linked to the cerebellum, thus are involved in
movement and posture.

Medulla Oblongata - is the structure of the caudal-most part of the brain stem, between the pons and spinal cord.
It is responsible for maintaining vital body functions, such as breathing, digestion and heartbeat.

B. Spinal Cord- A column of nerve tissue that runs from the base of the skull down the center of the
back. It is covered by the three thin layers of protective tissue called membranes. The spinal cord and
membranes are surrounded by the vertebrae (back bones). The spinal cord and the brain make up
the central nervous system. Spinal cord nerves carry messages between the brain and the rest of the
body. Spinal cord is about 18 inches long (45 centimeters). There are 31 pairs of spinal nerves and
roots.

The nerves of the spinal cord consist of:

 8 cervical nerves

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 12 thoracic nerves
 5 lumbar nerves
 5 sacral nerves
 1 coccygeal nerve

C. Neurons

Neurons are the building blocks of the CNS. Billions of these nerve cells can be found throughout the body
and communicate with one another to produce physical responses and actions.

Neurons are the body’s information superhighway. An estimated 86 billion neurons can be found in the
brain alone.

Most neurons are divided into 3 basic sections: dendrites, cell body and axon. These cells are differ in term
of functions. The three types of neurons are afferent neurons, efferent neurons and interneurons.

Efferent neurons are motor neurons that carry signals from the brain to the peripheral nervous
system. Afferent neurons are sensory neurons that bring information from the senses to the brain.
Interneurons are association neurons that connect efferent and afferent neurons to the CNS.

The neuron is made up of several components as follows:

 Cell body or Soma – this contains the nucleus, the neuron’s intracellular organelles (such as the
mitochondria and glial apparatus) and it is the location for cellular metabolism. It is also contains the
Nissl Substance. These are granules containing rough endoplasmic reticulum and free ribosomes,
making it the site of protein synthesis.
 Dendrites – these originate from the soma and extend outwards. They transmit signals they receive
from other neurons to the soma.
 Axon – It arises from the soma from an area called the axon hillock, where action potentials are
initiated. The action potentials are conducted through the axon to the axon terminal.
 Schwann cells – These insulate the axon which aids with rapid transmission of action potentials
through the axon.
 Axon terminal – Distally the axon branches to form axon terminals. These make synaptic connection
with other neurons. They contain various neurotransmitters which is released into the synapse to
allow signals to be transmitted from one neuron to the next.

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CELLS OF THE Nervous System

Glial Cells

Astrocytes

Astrocytes are star-shaped glial cells within the brain and spinal cord, depending on the method used they make
up between 20 and 40% of all glial cells. They have numerous functions, including:

 Providing metabolic support – The brain has a constant requirement for nutrients such glucose but they
are unable to store or produce glycogen themselves. This is overcome by the fact that astrocytes store
glycogen which can be broken down to glucose to provide fuel for neurons. Astrocytes can also store
lactate which is useful as a fuel during periods of high energy consumption or ischemia.
 Regulating the extracellular ionic environment – High-level of ions such as potassium can result in
spontaneous depolarization of the neuron. Astrocytes, thus, remove excess potassium ions from the
extracellular space.
 Neurotransmitter uptake – Astrocytes contain specific transporters for several neurotransmitters such
as glutamate. Rapid removal of neurotransmitters from the extracellular space is required for normal
function of neurons.
 Modulating synaptic transmission – In some regions of the brain, for example the hippocampus,
astrocytes release ATP in order to increase production of adenosine, which in turn inhibits synaptic
transmission
 Promotion of myelination by oligodendrocytes

Oligodendrocytes

These cells are responsible for insulating the axons in the central nervous system. They carry out this
function by producing a myelin sheath which wraps around a part of the axon.

A single oligodendrocyte has the capacity to myelinate up to 50 axonal segments. They are equivalent to the
Schwann cells in the peripheral nervous system.

6
Microglia

Microglial cells make up between 10 and 15% of cells within the brain and are of a mesodermal origin unlike
the other glial cells which are of ectodermal origin.

These cells are the phagocytic and immunocompetent cells of the nervous system. They are activated in
response to tissue damage and have the capability to recognize foreign antigens and initiate phagocytosis to
remove foreign material. If needed, microglia are also able to function as antigen presenting cells.

Ependymal cells

The ependyma is the thin lining of the ventricular system of the brain and spinal cord. This lining is made up
of ependymal cells, the basal membranes of which are attached to astrocytes. The main function of these
cells is the production of cerebrospinal fluid (CSF) as a part of the choroid plexus.

Their apical surfaces are covered with cilia and microvilli, which allow for the circulation and absorption of
CSF respectively.

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II. The Peripheral Nervous System (PNS).

The peripheral nervous system (PNS) is the division of the nervous system containing all the nerves that lie
outside of the central nervous system (CNS). The primary role of the PNS is to connect the CNS to the organs,
limbs, and skin. These nerves extend from the central nervous system to the outermost areas of the body.

The peripheral system allows the brain and spinal cord to receive and send information to other areas of
the body, which allows us to react to stimuli in our environment.

The nerves that make up the peripheral nervous system are actually the axons or bundles of axons from
nerve cells or neurons. In some cases, these nerves are very small but some nerve bundles are so large that
they can be easily seen by the human eye.

The peripheral nervous system itself is divided into two parts: the somatic nervous system and the
autonomic nervous system.

Each of these components plays a critical role in how the peripheral nervous system operates.

A. The Somatic Nervous System

The somatic system is the part of the peripheral nervous system responsible for carrying sensory and motor
information to and from the central nervous system. The somatic nervous system derives its name from the
Greek word soma, which means "body."

The somatic system is responsible for transmitting sensory information as well as for voluntary movement.
This system contains two major types of neurons:

 Motor neurons: Also called efferent neurons, motor neurons carry information from the brain and spinal
cord to muscle fibers throughout the body. These motor neurons allow us to take physical action in
response to stimuli in the environment.
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 Sensory neurons: Also called afferent neurons, sensory neurons carry information from the nerves to the
central nervous system. It is these sensory neurons that allow us to take in sensory information and send
it to the brain and spinal cord.
B. The Autonomic Nervous System

The autonomic system is the part of the peripheral nervous system that's responsible for regulating
involuntary body functions, such as blood flow, heartbeat, digestion, and breathing.

In other words, it is the autonomic system that controls aspects of the body that are usually not under
voluntary control. This system allows these functions to take place without needing to consciously think
about them happening. The autonomic system is further divided into two branches:

 Parasympathetic system - This helps maintain normal body functions and conserve physical
resources. Once a threat has passed, this system will slow the heart rate, slow breathing, reduce
blood flow to muscles, and constrict the pupils. This allows us to return our bodies to a normal
resting state.
 Sympathetic system - By regulating the flight-or-fight response, the sympathetic system prepares
the body to expend energy to respond to environmental threats. When action is needed, the
sympathetic system triggers a response by accelerating heart rate, increasing breathing rate,
boosting blood flow to muscles, activating sweat secretion, and dilating the pupils.

Synapses and neurotransmission

The nervous system is composed of billions of specialized cells called neurons. Efficient communication
between these cells is crucial to the normal functioning of the central and peripheral nervous system.

The cell body, or soma, of a neuron is like that of any other cell, containing mitochondria, ribosomes, a
nucleus, and other essential organelles. Extending from the cell membrane, however, is a system of dendritic
branches which serve as receptor sites for information sent from other neurons. If the dendrites receive a
strong enough signal from a neighboring nerve cell, or from several neighboring nerve cells, the resting
electrical potential of the receptor cell's membrane becomes depolarized. Regenerating itself, this electrical
signal travels down the cell's axon, a specialized extension from the cell body which ranges from a few
hundred micrometers in some nerve cells, to over a meter in length in others. This wave of depolarization
along the axon is called an action potential. Most axons are covered by myelin, a fatty substance that serves
as an insulator and thus greatly enhances the speed of an action potential. In between each sheath of myelin
is an exposed portion of the axon called a node of Ranvier. It is in these uninsulated areas that the actual
flow of ions along the axon takes place.

The end of the axon branches off into several terminals. Each axon terminal is highly specialized to pass along
action potentials to adjacent neurons, or target tissue, in the neural pathway. Some cells communicate this
information via electrical synapses. In such cases, the action potential simply travels from one cell to the next
through specialized channels, called gap junctions, which connect the two cells.

Most cells, however, communicate via chemical synapses. Such cells are separated by a space called a
synaptic cleft and thus cannot transmit action potentials directly. Instead, chemicals called neurotransmitters
are used to communicate the signal from one cell to the next. Some neurotransmitters are excitatory and
depolarize the next cell, increasing the probability that an action potential will be fired. Others are inhibitory,
causing the membrane of the next cell to hyperpolarize, thus decreasing the probability of that the next
neuron will fire an action potential.

The process by which this information is communicated is called synaptic transmission and can be broken
down into four steps. First, the neurotransmitter must be synthesized and stored in vesicles so that when an
action potential arrives at the nerve ending, the cell is ready to pass it along to the next neuron. Next, when
an action potential does arrive at the terminal, the neurotransmitter must be quickly and efficiently released
from the terminal and into the synaptic cleft. The neurotransmitter must then be recognized by selective
receptors on the postsynaptic cell so that it can pass along the signal and initiate another action potential.

9
Or, in some cases, the receptors act to block the signals of other neurons also connecting to that
postsynaptic neuron. After its recognition by the receptor, the neurotransmitter must be inactivated so that
it does not continually occupy the receptor sites of the postsynaptic cell. Inactivation of the
neurotransmitter avoids constant stimulation of the postsynaptic cell, while at the same time freeing up the
receptor sites so that they can receive additional neurotransmitter molecules, should another action
potential arrive.

Most neurotransmitters are specific for the kind of information that they are used to convey. As a result, a
certain neurotransmitter may be more highly concentrated in one area of the brain than it is in another. In
addition, the same neurotransmitter may elicit a variety of different responses based on the type of tissue
being targeted and which other neurotransmitters, if any, are co-released. The integral role of
neurotransmitters on the normal functioning of the brain makes it clear to see how an imbalance in any one
of these chemicals could very possibly have serious clinical implications for an individual. Whether due to
genetics, drug use, the aging process, or other various causes, biological disfunction at any of the four steps
of synaptic transmission often leads to such imbalances and is the ultimately source of conditions such as
schizophrenia, Parkinson's disease, and Alzheimer's disease.

Synaptic Transmission
Synaptic transmission is the process by which one neuron communicates with another. Information is passed
down the axon of the neuron as an electrical impulse known as action potential. Once the action potential
reaches the end of the axon it needs to be transferred to another neuron or tissue. It must cross over the
synaptic gap between the presynaptic neuron and post-synaptic neuron. At the end of the neuron (in the
axon terminal) are the synaptic vesicles, which contain chemical messengers, known as neurotransmitters.
When the electrical impulse (action potential) reaches these synaptic vesicles, they release their contents of
neurotransmitters. Neurotransmitters then carry the signal across the synaptic gap. They bind to receptor
sites on the post-synaptic cell, thereby completing the process of synaptic transmission.

V. Materials/Devices:

1. Laptop
2. Mobile Phone

VI. Teaching Methodologies:

Lecture/Discussion

Power Point Presentations

Short Video

VII. Assessment:

Quiz

VIII. Activity:

Draw a schematic representation of the central nervous system

Resources:

Pinel, John P. (2011), Inc., Biopsychology, 8th ed,. Pearson, Education, Inc.,

Brown, Thomas S. & Wallace, Patricia M (1980) Physiological Psychology. Elsevie , Inc.,
https://web.williams.edu/imput/introduction_main.html?
fbclid=IwAR1TKcmXkgKFHIY44Lv0h-fjmzTaYKtJ-wfqFsl4uYI-1syy9k-HnURO
Module 2
10
This module includes how the brain allows us to see hear, feel, taste and smell, as well as how neuronal networks in
the brain and spinal cord plan, initiate and execute movements.

I. Learning Outcomes:

At the end of the topic, the students should be able to:

1. Describe the organization of motor neuron pathways.


2. Explain the role does the brain play in the sensory system.

II. Topic 2. Sensory and Motor System


2.1 Sensory System
2.1.1 Sight
2.1.2 Hearing
2.1.3 Taste
2.1.4 Smell
2.1.5 Touch
2.2 Motor System
2.2.1 Organization of Motor Neuron Pathways
2.2.1.1 The Role of Basal Ganglia in Movement
2.2.1.2 Modulation of Movement by the Cerebellum
III. Time Frame: Week 3

IV. Topic Discussion:

The Sensory and Motor System

Sensory System

Sight. Sight probably tells us more about the world than any other sense. Light entering the eye forms an
upside-down image on the retina. The retina transforms the light into nerve signals for the brain. The brain
then turns the image right-side up and tells us what we are seeing.

Hearing. Every sound we hear is the result of sound waves entering our ears and making our eardrums
vibrate. These vibrations then move along the tiny bones of the middle ear and turned into nerve signals. The
cortex processes these signals, telling us what we're hearing.

Taste. The tongue contains small groups of sensory cells called taste buds that react to chemicals in foods.
Taste buds react to sweet, sour, salty, bitter, and savory. The taste buds send messages to the areas in the
cortex responsible for processing taste.

Smell. Olfactory cells in the mucous membranes lining each nostril react to chemicals we breathe in and send
messages along specific nerves to the brain.

Touch. The skin contains millions of sensory receptors that gather information related to touch, pressure,
temperature, and pain and send it to the brain for processing and reaction.

Motor System

11
Organization of Motor Neuron Pathways

The motor system is the part of the central nervous system that is involved with movement. It consists of the
pyramidal and extrapyramidal system.

The motor pathway, also called the pyramidal tract or the corticospinal tract, serves as the motor pathway
for upper motor neuronal signals coming from the cerebral cortex and from primitive brainstem motor
nuclei. There are upper and lower motor neurons in the corticospinal tract.

The motor impulses originate in the giant pyramidal cells (Betz cells) of the motor area, i.e., the precentral
gyrus of the cerebral cortex. These are the upper motor neurons of the corticospinal tract. The axons of
these cells pass from the cerebral cortex to the midbrain and the medulla oblongata. Peripheral motor
nerves carry the motor impulses from the anterior horn to the voluntary muscles.

Cortical upper motor neurons originate from Brodmann areas 1, 2, 3, 4, and 6, then descend into the
posterior limb of the internal capsule, through the crus cerebri, down through the pons, and to the medullary
pyramids, where about 90% of the axons cross to the contralateral side at the decussation of the pyramids.
They then descend as the lateral corticospinal tract.

These axons synapse with lower motor neurons in the ventral horns of all levels of the spinal cord. The
remaining 10% of axons descend on the ipsilateral side as the ventral corticospinal tract. These axons also
synapse with lower motor neurons in the ventral horns. Most of them will cross to the contralateral side of
the cord (via the anterior white commissure) just before synapsing.

Brodmann areas of the brain: This drawing shows the regions of the human cerebral cortex as delineated by
Korvinian Brodmann on the basis of cytoarchitecture.

The midbrain nuclei include four motor tracts that send upper motor neuronal axons down the spinal cord to
lower motor neurons. These are the rubrospinal tract, the vestibulospinal tract, the tectospinal tract, and the
reticulospinal tract.

The function of lower motor neurons can be divided into two different groups: the lateral corticospinal tract
and the anterior corticalspinal tract. The lateral tract contains upper motor neuronal axons that synapse on
the dorsal lateral lower motor neurons, which are involved in distal limb control.

The anterior corticospinal tract descends ipsilaterally in the anterior column, where the axons emerge and
either synapse on ventromedial lower motor neurons in the ventral horn ipsilaterally or descussate at the
anterior white commissure where they synapse on ventromedial lower motor neurons contralaterally.

The ventromedial lower motor neurons control the large, postural muscles of the axial skeleton. These lower
motor neurons, unlike those of the dorsal lateral, are located in the ventral horn throughout the spinal cord.

12
Spinal cord tracts: This diagram of spinal cord tracts shows the motor and efferent pathways in red and
the sensory and afferent pathways in blue. Included in the diagram are the following motor pathways:
corticospinal tracts (pyramidal tract), and extrapyramidal tracts (tectospinal tract not delineated).

The Role of the Basal Ganglia in Movement

The basal ganglia are responsible for voluntary motor control, procedural learning, and eye movement, as
well as cognitive and emotional functions.

Location of the Basal Ganglia

The basal ganglia (or basal nuclei) are a group of nuclei of varied origin in the brains of vertebrates that act as
a cohesive functional unit. They are situated at the base of the forebrain and are strongly connected with the
cerebral cortex, thalamus, and other brain areas.

The basal ganglia are associated with a variety of functions, including voluntary motor control, procedural
learning relating to routine behaviors or habits such as bruxism and eye movements, as well as cognitive
and emotional functions.

13
Basal ganglia: Locations of the basal ganglia.

Action Selection

Currently popular theories hold that the basal ganglia play a primary role in action selection. Action selection
is the decision of which of several possible behaviors to execute at a given time.

Experimental studies show that the basal ganglia exert an inhibitory influence on a number of motor
systems, and that a release of this inhibition permits a motor system to become active. The behavior
switching that takes place within the basal ganglia is influenced by signals from many parts of the brain,
including the prefrontal cortex, which plays a key role in executive functions.

Movement

The greatest source of insight into the functions of the basal ganglia has come from the study of two
neurological disorders, Parkinson’s disease and Huntington’s disease. For both of these disorders, the nature
of the neural damage is well-understood and can be correlated with the resulting symptoms.

Parkinson’s disease involves the major loss of dopaminergic cells in the substantia nigra. Huntington’s
disease involves the massive loss of medium spiny neurons in the striatum.

The symptoms of the two diseases are virtually opposite: Parkinson’s disease is characterized by a gradual
loss of the ability to initiate movement, whereas Huntington’s disease is characterized by an inability to
prevent parts of the body from moving unintentionally.

It is noteworthy that, although both diseases have cognitive symptoms, especially in their advanced stages,
the most salient symptoms relate to the ability to initiate and control movement. Thus, both are classified
primarily as movement disorders.

A different movement disorder, called hemiballismus, may result from damage restricted to the subthalamic
nucleus. Hemiballismus is characterized by violent and uncontrollable flinging movements of the arms and
legs.

Function in Eye Movement

14
One of the most intensively studied functions of the basal ganglia is their role in controlling eye movements.
Eye movement is influenced by an extensive network of brain regions that converge on a midbrain area
called the superior colliculus (SC).

The SC is a layered structure whose layers form two-dimensional retinotopic maps of visual space. A bump of
neural activity in the deep layers of the SC drives eye movement toward the corresponding point in space.

Motivation

Although the role of the basal ganglia in motor control is clear, there are also many indications that it is
involved in the control of behavior in a more fundamental way, at the level of motivation. In Parkinson’s
disease, the ability to execute the components of movement is not greatly affected, but motivational factors
such as hunger fail to cause movements to be initiated or switched at the proper times.

The immobility of patients with Parkingson’s disease has sometimes been described as a paralysis of the will.
These patients have occasionally been observed to show a phenomenon called kinesia paradoxica, in which a
person who is otherwise immobile responds to an emergency in a coordinated and energetic way, then
lapses back into immobility once the emergency has passed.

The role in motivation of the limbic part of the basal ganglia—the nucleus accumbens (NA), ventral pallidum,
and ventral tegmental area (VTA)—is particularly well established. Thousands of experimental studies
combine to demonstrate that the dopaminergic projection from the VTA to the NA plays a central role in the
brain’s reward system.

Numerous things that people find rewarding, including addictive drugs, good-tasting food, and sex, have
been shown to elicit activation of the VTA dopamine system. Damage to the NA or VTA can produce a state
of profound torpor.

Neurotransmitters

In most regions of the brain, the predominant classes of neurons use glutamate as the neurotransmitter and
have excitatory effects on their targets. In the basal ganglia, however, the great majority of neurons uses
gamma-aminobutyric acid (GABA) as the neurotransmitter and have inhibitory effects on their targets.

The inputs from the cortex and thalamus to the striatum and subthalamic nucleus are glutamatergic, but the
outputs from the striatum, pallidum, and substantia nigra pars reticulata all use GABA. Thus, following the
initial excitation of the striatum, the internal dynamics of the basal ganglia are dominated by inhibition and
disinhibition.

Other neurotransmitters have important modulatory effects. Dopamine is used by the projection from the
substantia nigra pars compacta to the dorsal striatum and also in the analogous projection from the ventral
tegmental area to the ventral striatum (nucleus accumbens).

Acetylcholine also plays an important role, as it is used both by several external inputs to the striatum and by
a group of striatal interneurons. Although cholinergic cells make up only a small fraction of the total
population, the striatum has one of the highest acetylcholine concentrations of any brain structure.

Modulation of Movement by the Cerebellum

The cerebellum is important for motor control—specifically coordination, precision, and timing—as well as
some forms of motor learning.

the cerebellum is a region of the brain that plays an important role in motor control. It may also be involved
in some cognitive functions such as attention and language, and in regulating fear and pleasure responses,
but its movement-related functions are the most solidly established. The cerebellum does not initiate
movement, but it contributes to coordination, precision, and accurate timing.

15
It receives input from sensory systems of the spinal cord and from other parts of the brain, including the
cerebral cortex, and integrates these inputs to fine-tune motor activity. Because of this fine-tuning function,
damage to the cerebellum does not cause paralysis, but instead produces disorders in fine movement,
equilibrium, posture, and motor learning.

The cerebellum differs from most other parts of the brain, especially the cerebral cortex, in regards to the
ability of signals to move unidirectionally from input to output. This feedforward mode of operation means
that the cerebellum cannot generate self-sustaining patterns of neural activity, in contrast to the cerebral
cortex. However, the cerebellum can receive information from the cerebral cortex and processes this
information to send motor impulses to the skeletal muscle.

Anatomy of the Cerebellum

In terms of anatomy, the cerebellum has the appearance of a separate structure attached to the bottom of the
brain, tucked underneath the cerebral hemispheres. The surface of the cerebellum is covered with finely spaced
parallel grooves, in striking contrast to the broad irregular convolutions of the cerebral cortex. These parallel grooves
conceal the fact that the cerebellum is actually a continuous thin layer of tissue (the cerebellar cortex), tightly folded
in the style of an accordion.

Within this thin layer are several types of neurons with a highly regular arrangement, the most important being
Purkinje cells and granule cells. This complex neural network gives rise to a massive signal-processing capability, but
almost all of its output is directed to a set of small, deep cerebellar nuclei lying in the interior of the cerebellum.

Function

Marr-Albus Theory

In addition to its direct role in motor control, the cerebellum is also necessary for several types of motor learning, the
most notable one being learning to adjust to changes in sensorimotor relationships.

Several theoretical models have been developed to explain sensorimotor calibration in terms of synaptic plasticity
within the cerebellum. Most of them derive from early models formulated by David Marr and James Albus, which
were motivated by the observation that each cerebellar Purkinje cell receives two dramatically different types of
input.

16
It receives input from thousands of parallel fibers, each individually very weak. However, each cerebellar Purkinje cell
also gets input from one single climbing fiber, which is so strong that a single climbing fiber action potential will
reliably cause a target Purkinje cell to fire a burst of action potentials.

The basic concept of the Marr-Albus theory is that the climbing fiber serves as a teaching signal, which induces a
long-lasting change in the strength of synchronously activated parallel fiber inputs. Observations of long-term
depression in parallel fiber inputs have provided support for theories of this type, but their validity remains
controversial.

Insights from Cerebellar Dysfunction

The strongest clues to the function of the cerebellum have come from examining the consequences of damage to it.
Animals and humans with cerebellar dysfunction show, above all, problems with motor control. They continue to be
able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed
movements.

A standard test of cerebellar function is to reach with the tip of the finger for a target at arm’s length. A healthy
person will move the fingertip in a rapid straight trajectory, whereas a person with cerebellar damage will reach
slowly and erratically, with many mid-course corrections.

Deficits in non-motor functions are more difficult to detect. Thus, the general conclusion reached decades ago is that
the basic function of the cerebellum is not to initiate movements, or to decide which movements to execute, but
rather to calibrate the detailed form of a movement.

The comparative simplicity and regularity of the cerebellar anatomy led to an early hope that it might imply a similar
simplicity of computational function. Although a full understanding of cerebellar function remains elusive, at least
four principles are identified as important: 1) feedforward processing, 2) divergence and convergence, 3) modularity,
and 4) plasticity.

 Feedforward processing: Refers to the unidirectional movement of signals through the system from input to
output, with very little recurrent internal transmission. This means that the cerebellum, in contrast to the
cerebral cortex, cannot generate self-sustaining patterns of neural activity. Signals enter the circuit, are
processed by each stage in sequential order, and then leave.
 Divergence and convergence: The 1000 or so Purkinje cells belonging to a microzone may receive input from
as many as 100 million parallel fibers, and focus their own output down to a group of less than 50 deep
nuclear cells. Thus, the cerebellar network receives a modest number of inputs, processes them very
extensively through its rigorously structured internal network, and sends out the results via a very limited
number of output cells.
 Modularity: The cerebellar system is functionally divided into independent modules. All modules have a
similar internal structure, but with different inputs and outputs. The output of one module does not appear
to significantly influence the activity of other modules
 Plasticity: The synapses between parallel fibers and Purkinje cells, and the synapses between mossy fibers
and deep nuclear cells, are both susceptible to modification of their strength. The influence of each parallel
fiber on nuclear cells is adjustable. This arrangement gives tremendous flexibility for fine-tuning the
relationship between the cerebellar inputs and outputs.

Functions of the Cerebellum in Integrating Movements

The cerebellum uses feedforward processing and modularity to process information.

Cerebellar Function

Feedforward Processing

The cerebellum differs from most other parts of the brain in that the signal processing is almost entirely feed
forward—that is, signals move unidirectionally through the system from input to output, with very little recurrent
internal transmission.

17
The small amount of recurrence that does exist consists of mutual inhibition; there are no mutually excitatory
circuits. This feedforward mode of operation means that the cerebellum, in contrast to the cerebral cortex, cannot
generate self-sustaining patterns of neural activity.

Signals enter the circuit, are processed by each stage in sequential order, and then leave. As Eccles, Ito, and
Szentágothai wrote,”This elimination in the design of all possibility of reverberatory chains of neuronal excitation is
undoubtedly a great advantage in the performance of the cerebellum as a computer, because what the rest of the
nervous system requires from the cerebellum is presumably not some output expressing the operation of complex
reverberatory circuits in the cerebellum, but rather a quick and clear response to the input of any particular set of
information.”

Divergence and Convergence

Cells of the Cerebellum: Transverse section of a cerebellar folium, showing its principal cell types and connections.

In the human cerebellum, information from 200 million mossy fiber inputs is expanded to 40 billion granule cells,
whose parallel fiber outputs then converge onto 15 million Purkinje cells. Because of the way that they are lined up
longitudinally, the 1,000 or so Purkinje cells belonging to a microzone may receive input from as many as 100 million
parallel fibers and focus their own output down to a group of less than 50 deep nuclear cells.

Thus, the cerebellar network receives a modest number of inputs, processes them very extensively through its
rigorously structured internal network, and sends out the results via a very limited number of output cells.

Modularity

The cerebellar system is functionally divided into more or less independent modules, that probably number in the
hundreds to thousands. All modules have a similar internal structure, but different inputs and outputs.

18
A module (a multizonal microcompartment in the terminology of Apps and Garwicz) consists of a small cluster of
neurons in the inferior olivary nucleus, a set of long narrow strips of Purkinje cells in the cerebellar cortex
(microzones), and a small cluster of neurons in one of the deep cerebellar nuclei.

Different modules share input from mossy fibers and parallel fibers, but in other respects they appear to function
independently. The output of one module does not appear to significantly influence the activity of other modules.

Plasticity

The synapses between parallel fibers and Purkinje cells, and the synapses between mossy fibers and deep nuclear
cells, are both susceptible to modification of their strength. In a single cerebellar module, input from as many as a
billion parallel fibers converge onto a group of less than 50 deep nuclear cells, and the influence of each parallel fiber
on those nuclear cells is adjustable. This arrangement gives tremendous flexibility for fine-tuning the relationships
between the cerebellar inputs and outputs.

Zones and microzones in the cerebellum: This schematic illustration of the structure of zones and microzones in the
cerebellum shows three levels of magnification. These zones and microzones help explain the modular nature of the
cerebellar function. On the left is a simplified illustration of what the cerebellar cortex would look like if all the folds
were straightened out—the vertical dimension is the rostro-caudal axis of the cerebellum, the horizontal dimension
is the medio-lateral axis. A zone is a longitudinally oriented strip of the cortex, and a microzone is a thin,
longitudinally oriented portion of a zone. As the illustration on the right shows, Purkinje cell dendritic trees are
flattened in a way that aligns with the microzone length, and parallel fibers cross the microzones at right angles.

19
V. Materials/Devices:

1. Laptop
2. Mobile Phone

VI. Teaching Methodologies:

Lecture/Discussion

Group Reporting

Short Video

Power Point Presentations

VII. Assessment:

Quiz

Graded Recitation

VIII. Activity:

 Draw the locations of the basal ganglia


 Explain the role of basal ganglia in voluntary motor control

Resources:

Pinel, John P. (2011), Inc., Biopsychology, 8th ed,. Pearson, Education, Inc.,

Shapero, Martin S. (2019), Biopsychology Fundamentals and Temporary Issues.


https://opentextbc.ca/anatomyandphysiologyopenstax/chapter/the-sensory-and-motor-
exams/?
fbclid=IwAR36UALp7PlSHMtKwLBuSVARcyxmuJ5gvnKzqSDpmnHAee_Ad1VNe1bYQw8#fig-
ch16_04_02

20
Module 3

This module discusses the role of the nervous system in voluntary and involuntary movements

I. Learning Outcomes:

At the end of the topic, the students should be able to:

1. Describe which muscles are responsible for voluntary and involuntary movements
2. Cite examples on voluntary and involuntary movements

II. Topic 3. Movements


3.1 Voluntary Movements
3.2 Involuntary Movements
III. Time Frame: Week 4

IV. Topic Discussion:

The Motor Cortex

All of the body's voluntary movements are controlled by the brain. One of the brain areas most involved in
controlling these voluntary movements is the motor cortex.

The motor cortex is located in the rear


portion of the frontal lobe, just before the
central sulcus (furrow) that separates the
frontal lobe from the parietal lobe. The
motor cortex is divided into two main
areas, Area 4 and Area 6. Area 4, also
known as the primary motor cortex, forms
a thin band along the central sulcus. Area
6 lies immediately forward of Area 4. Area
6 is wider and is further subdivided into
two distinct sub-areas.

To carry out goal-directed movements, your motor cortex must first receive various kinds of information from
the various lobes of the brain: information about the body's position in space, from the parietal lobe; about the goal
to be attained and an appropriate strategy for attaining it, from the anterior portion of the frontal lobe; about
memories of past strategies, from the temporal lobe; and so on.

21
In 1870, Hitzig and Fritsch electrically stimulated various parts of
a dog's motor cortex. They observed that depending on what part
of the cortex they stimulated, a different part of the body
contracted. Then they found that if they destroyed this same
small area of the cortex, the corresponding part of the body
became paralyzed. This is how it was discovered that every part
of the body has a particular region of the primary motor cortex
that controls its movement.

But what is remarkable about this "motor map" is that certain


parts of the body—those that can make the finest movements—
take up much more space than others. These parts of the body
are shown larger than the others in the illustration here.

The Basal Ganglia

As their name suggests, the basal


ganglia consist of a set of neural
structures buried deep inside the cerebrum.
The main basal ganglia are the caudate
nucleus, the putamen, and the globus pallidus.

These ganglia, or clusters of nerve cells, are tightly interconnected. They also receive information from several
different regions of the cerebral cortex. Once the basal ganglia have processed this information, they return it to the
motor cortex via the thalamus.

One of the likely functions of this loop, which operates in conjunction with another one involving the cerebellum, is
to select and trigger well coordinated voluntary movements.

This role of the basal ganglia in initiating and regulating motor commands becomes clearly apparent in people whose
basal ganglia have been damaged, such as patients with Parkinson's disease. These patients display difficulty in
starting the movements they have planned, as well as trembling and slowness once they do begin them.

22
The Cerebellum

For you to perform even so simple a


gesture as touching the tip of your nose, it
is not enough for your brain to simply
command your hand and arm muscles to
contract. To make the various segments of
your hand and arm deploy smoothly, you
need an internal "clock" that can precisely
regulate the sequence and duration of the
elementary movements of each of these
segments. That clock is the cerebellum.

As so often in neurobiology, to understand exactly what the cerebellum does, we can observe patients in whom part
of this structure has been destroyed (by a tumour or a stroke, for example). When these patients try to grasp an
object, their hands start moving late, advance unsteadily, and either stop before reaching their target, or, often,
accelerate past it. In terms of posture, people with damaged cerebellums characteristically display balance problems
similar to those found in people who are drunk. In fact, the clumsiness that accompanies excess consumption
of alcohol is directly related to its depressive effects on the activity of the cerebellum.

In a healthy person, the cerebellum first receives


information about the intended movement from
the sensory and motor cortexes. Then it sends
information back to the motor cortex about the
required direction, force, and duration of this
movement Thus this loop involving the
cerebellum operates in addition to the loop
involving the basal ganglia to regulate the details of
motor control.

Another metaphor summarizes the role of your cerebellum rather well: it acts like an air traffic controller who
gathers an unbelievable amount of information at every moment, including (to return to our original example) the
position of your hand, your arm, and your nose, the speed of their movements, and the effects of potential obstacles
in their path, so that your finger can achieve a "soft landing" on the tip of your nose.

The Activation Sequence for The Motor Areas

The basic function of the brain is to produce behavior, which are, first and foremost, movements. Several different
regions of the cerebral cortex are involved in controlling the body's movements.

These regions are organized into a hierarchy like the crew of a ship. On an ancient galley, for example, the captain
determined the destination for a voyage by assessing the various factors that might make such a trip worthwhile.
Then his lieutenants calculated the direction that the ship had to travel to reach that destination, based on weather

23
conditions. Finally, the lieutenants transmitted their orders to the crew manning the oars, who used their muscles to
move the ship in the desired direction.

Similarly, in the human brain, planning for any given


movement is done mainly in the forward portion of the
frontal lobe. This part of the cortex receives information
about the individual's current position from several other
parts. Then, like the ship's captain, it issues its commands, to
Area 6. Area 6 acts like the ship's lieutenants. It decides which
set of muscles to contract to achieve the required movement,
then issues the corresponding orders to the "rowers"—the
primary motor cortex, also known as Area 4. This area in turn
activates specific muscles or groups of muscles via the motor
neurons in the spinal cord.

Even for a movement as simple as picking up a glass of water, one can scarcely imagine trying to consciously specify
the sequence, force, amplitude, and speed of the contractions of every muscle concerned. And yet, if we are healthy,
we all make such movements all the time without even thinking of them.

The decision to pick up a glass of water is accompanied by increased electrical activity in the frontal region of the
cortex. The neurons in the frontal cortex then send impulses down their axons to activate the motor cortex itself.
Using the information supplied by the visual cortex, the motor cortex plans the ideal path for the hand to follow to
reach the glass. The motor cortex then calls on other parts of the brain, such as the central grey nuclei and the
cerebellum, which help to initiate and co-ordinate the activation of the muscles in sequence.

The axons of the neurons of the primary motor cortex descend all the way into the spinal cord, where they make the
final relay of information to the motor neurons of the spinal cord. These neurons are connected directly to the
muscles and cause them to contract. Finally, by contracting and by thus pulling on the bones of the arm and hand,
the muscles execute the movement that enables the glass to be picked up.

In addition, to ensure that all of these movements are fast, precise, and co-ordinated, the nervous system must
constantly receive sensory information from the outside world and use this information to adjust and correct the
hand's trajectory. The nervous system achieves these adjustments chiefly by means of the cerebellum, which
receives information about the positions in space of the joints and the body from the proprioceptors.

Despite its protective coverings, the brain is still a vulnerable organ. Repeated blows can cause permanent damage
over time, and a single severe blow, even if it doesn't crack the skull or damage the brain, can disrupt the brain's
normal operation and knock the victim unconscious [sound of heart beating]. Thinking ceases. Conscious control of
muscle is lost. Sensory information is not heeded, and yet the heart continues to beat and the lungs to draw air.

These vital mechanisms are controlled by one of the brain's most durable parts--the brain stem. The brain stem is an
automatic control center for many such important involuntary actions of the body. And, it is a pathway for impulses
travelling back and forth between the body and the rest of the brain.

Consider the body as a kind of machine with certain basic actions that must be maintained and coordinated no
matter what the state of our mind. The brain stem helps serve this purpose. It regulates heartbeat and respiration. It
helps to wake up the rest of the brain from sleep by activating the other areas. It regulates blood pressure moment
by moment. If it failed to do so, we would faint every time we stood up. It controls certain reflex actions such as
blinking and the adjustment of the eyes to varying light. It guides involuntary actions necessary for eating such as the
production of saliva and coordination of the muscles used to swallow. We are then free to think about other things,
24
but it will not allow us to neglect the body's basic needs when the time comes. For example, if food goes down the
wrong way, the brain stem will force us to cough. If the brain stem is damaged, the repercussions can be severe--
paralysis, coma, death.

V. Materials/Devices:

1. Laptop
2. Mobile Phone

VI. Teaching Methodologies:

Lecture/Discussion

Active class participation

Short video

Power Point Presentations

Group Reporting

VII. Assessment:

Quiz

Graded Recitation

VIII. Activity:

Group video presentation on voluntary movements

Resources:

Pinel, John P. (2011), Inc., Biopsychology, 8th ed,. Pearson, Education, Inc.,

Brown, Thomas S. & Wallace, Patricia M (1980) Physiological Psychology. Elsevie , Inc.,
https://www.britannica.com/video/81386/brainstem-actions-control-centre-body-blood-
pressure?
fbclid=IwAR36UALp7PlSHMtKwLBuSVARcyxmuJ5gvnKzqSDpmnHAee_Ad1VNe1bYQw8
https://thebrain.mcgill.ca/flash/d/d_06/d_06_cr/d_06_cr_mou/d_06_cr_mou.html?
fbclid=IwAR3nyrY4o4imC2u8NLxeAzdr5VkOG25kvCn1_mJRMzDYd3cayGIkrKNoX3s

25
Module 4

This module covers sleep and wake cycles generated by central nervous system.

I. Learning Outcomes:

At the end of the topic, the students should be able to:

1. Discuss the function of endogenous rhythms and difficulty with altered rhythms
2. Identify the various sleep disorders, their causes, their treatments and drugs that affect
sleep.

II. Topic 4. Sleep and Biological Rhythms


4.1 Anatomy of Sleep
4.2 Stages of Sleep
4.3 Sleep Mechanics
4.4 Importance of Sleep
4.5 Effects of Sleep Deprivation
4.6 Sleep Disorders
4.7 Effects of Long Term Sleep Deprivation
4.8 Drugs that Affect sleep
III. Time Frame: Week 5-6

IV. Topic Discussion:

Anatomy of Sleep

Several structures within the brain are involved with sleep.

The hypothalamus, a peanut-sized structure deep inside the brain, contains groups of nerve cells that act as control
centers affecting sleep and arousal. Within the hypothalamus is the suprachiasmatic nucleus (SCN) – clusters of
thousands of cells that receive information about light exposure directly from the eyes and control your behavioral
rhythm. Some people with damage to the SCN sleep erratically throughout the day because they are not able to
match their circadian rhythms with the light-dark cycle. Most blind people maintain some ability to sense light and
are able to modify their sleep/wake cycle.

The brain stem, at the base of the brain, communicates with the hypothalamus to control the transitions between
wake and sleep. (The brain stem includes structures called the pons, medulla, and midbrain.) Sleep-promoting cells
within the hypothalamus and the brain stem produce a brain chemical called GABA, which acts to reduce the activity
of arousal centers in the hypothalamus and the brain stem. The brain stem (especially the pons and medulla) also
plays a special role in REM sleep; it sends signals to relax muscles essential for body posture and limb movements, so
that we don’t act out our dreams.

The thalamus acts as a relay for information from the senses to the cerebral cortex (the covering of the brain that
interprets and processes information from short- to long-term memory). During most stages of sleep, the thalamus
becomes quiet, letting you tune out the external world. But during REM sleep, the thalamus is active, sending the
cortex images, sounds, and other sensations that fill our dreams.

The pineal gland, located within the brain’s two hemispheres, receives signals from the SCN and increases production
of the hormone melatonin, which helps put you to sleep once the lights go down. People who have lost their sight
and cannot coordinate their natural wake-sleep cycle using natural light can stabilize their sleep patterns by taking
small amounts of melatonin at the same time each day. Scientists believe that peaks and valleys of melatonin over
time are important for matching the body’s circadian rhythm to the external cycle of light and darkness.

The basal forebrain, near the front and bottom of the brain, also promotes sleep and wakefulness, while part of
the midbrain acts as an arousal system. Release of adenosine (a chemical by-product of cellular energy
26
consumption) from cells in the basal forebrain and probably other regions supports your sleep drive. Caffeine
counteracts sleepiness by blocking the actions of adenosine.

The amygdala, an almond-shaped structure involved in processing emotions, becomes increasingly active during REM
sleep.

Stages of Sleep

There are two basic types of sleep: rapid eye movement (REM) sleep and non-REM sleep (which has three different
stages). Each is linked to specific brain waves and neuronal activity. You cycle through all stages of non-REM and
REM sleep several times during a typical night, with increasingly longer, deeper REM periods occurring toward
morning.

Stage 1 non-REM sleep is the changeover from wakefulness to sleep. During this short period (lasting several
minutes) of relatively light sleep, your heartbeat, breathing, and eye movements slow, and your muscles relax with
occasional twitches. Your brain waves begin to slow from their daytime wakefulness patterns.

Stage 2 non-REM sleep is a period of light sleep before you enter deeper sleep. Your heartbeat and breathing slow,
and muscles relax even further. Your body temperature drops and eye movements stop. Brain wave activity slows
but is marked by brief bursts of electrical activity. You spend more of your repeated sleep cycles in stage 2 sleep
than in other sleep stages.

Stage 3 non-REM sleep is the period of deep sleep that you need to feel refreshed in the morning. It occurs in longer
periods during the first half of the night. Your heartbeat and breathing slow to their lowest levels during sleep. Your
muscles are relaxed and it may be difficult to awaken you. Brain waves become even slower.

REM sleep first occurs about 90 minutes after falling asleep. Your eyes move rapidly from side to side behind closed
eyelids. Mixed frequency brain wave activity becomes closer to that seen in wakefulness. Your breathing becomes
faster and irregular, and your heart rate and blood pressure increase to near waking levels. Most of your dreaming
occurs during REM sleep, although some can also occur in non-REM sleep. Your arm and leg muscles become
temporarily paralyzed, which prevents you from acting out your dreams. As you age, you sleep less of your time in
REM sleep. Memory consolidation most likely requires both non-REM and REM sleep.

Sleep Mechanism

Two internal biological mechanisms–circadian rhythm and homeostasis–work together to regulate when you are
awake and sleep.

Circadian rhythms direct a wide variety of functions from daily fluctuations in wakefulness to body temperature,
metabolism, and the release of hormones. They control your timing of sleep and cause you to be sleepy at night and
your tendency to wake in the morning without an alarm. Your body’s biological clock, which is based on a roughly
24-hour day, controls most circadian rhythms. Circadian rhythms synchronize with environmental cues (light,
temperature) about the actual time of day, but they continue even in the absence of cues.

Sleep-wake homeostasis keeps track of your need for sleep. The homeostatic sleep drive reminds the body to sleep
after a certain time and regulates sleep intensity. This sleep drive gets stronger every hour you are awake and causes
you to sleep longer and more deeply after a period of sleep deprivation.

Factors that influence your sleep-wake needs include medical conditions, medications, stress, sleep environment,
and what you eat and drink. Perhaps the greatest influence is the exposure to light. Specialized cells in the retinas of
your eyes process light and tell the brain whether it is day or night and can advance or delay our sleep-wake cycle.
Exposure to light can make it difficult to fall asleep and return to sleep when awakened.

Night shift workers often have trouble falling asleep when they go to bed, and also have trouble staying awake at
work because their natural circadian rhythm and sleep-wake cycle is disrupted. In the case of jet lag, circadian
rhythms become out of sync with the time of day when people fly to a different time zone, creating a mismatch
between their internal clock and the actual clock.

27
Importance of Sleep
Sleep is an important part of your daily routine—you spend about one-third of your time doing it. Quality
sleep – and getting enough of it at the right times -- is as essential to survival as food and water. Without
sleep you can’t form or maintain the pathways in your brain that let you learn and create new memories, and
it’s harder to concentrate and respond quickly.

Sleep is important to a number of brain functions, including how nerve cells (neurons) communicate with
each other. In fact, your brain and body stay remarkably active while you sleep. Recent findings suggest that
sleep plays a housekeeping role that removes toxins in your brain that build up while you are awake.

Everyone needs sleep, but its biological purpose remains a mystery. Sleep affects almost every type of tissue
and system in the body – from the brain, heart, and lungs to metabolism, immune function, mood, and
disease resistance. Research shows that a chronic lack of sleep, or getting poor quality sleep, increases the
risk of disorders including high blood pressure, cardiovascular disease, diabetes, depression, and obesity.

Sleep is a complex and dynamic process that affects how you function in ways scientists are now beginning to
understand. This booklet describes how your need for sleep is regulated and what happens in the brain
during sleep.

The hypothalamus, a peanut-sized structure deep inside the brain, contains groups of nerve cells that act as
control centers affecting sleep and arousal. Within the hypothalamus is the suprachiasmatic nucleus (SCN) –
clusters of thousands of cells that receive information about light exposure directly from the eyes and
control your behavioral rhythm. Some people with damage to the SCN sleep erratically throughout the day
because they are not able to match their circadian rhythms with the light-dark cycle. Most blind people
maintain some ability to sense light and are able to modify their sleep/wake cycle.

The brain stem, at the base of the brain, communicates with the hypothalamus to control the transitions
between wake and sleep. (The brain stem includes structures called the pons, medulla, and midbrain.)
Sleep-promoting cells within the hypothalamus and the brain stem produce a brain chemical called GABA,
which acts to reduce the activity of arousal centers in the hypothalamus and the brain stem. The brain stem
(especially the pons and medulla) also plays a special role in REM sleep; it sends signals to relax muscles
essential for body posture and limb movements, so that we don’t act out our dreams.

The thalamus acts as a relay for information from the senses to the cerebral cortex (the covering of the brain
that interprets and processes information from short- to long-term memory). During most stages of sleep,
the thalamus becomes quiet, letting you tune out the external world. But during REM sleep, the thalamus is
active, sending the cortex images, sounds, and other sensations that fill our dreams.

The pineal gland, located within the brain’s two hemispheres, receives signals from the SCN and increases
production of the hormone melatonin, which helps put you to sleep once the lights go down. People who
have lost their sight and cannot coordinate their natural wake-sleep cycle using natural light can stabilize
their sleep patterns by taking small amounts of melatonin at the same time each day. Scientists believe that
peaks and valleys of melatonin over time are important for matching the body’s circadian rhythm to the
external cycle of light and darkness.

The basal forebrain, near the front and bottom of the brain, also promotes sleep and wakefulness, while part
of the midbrain acts as an arousal system. Release of adenosine (a chemical by-product of cellular energy
consumption) from cells in the basal forebrain and probably other regions supports your sleep drive.
Caffeine counteracts sleepiness by blocking the actions of adenosine.

The amygdala, an almond-shaped structure involved in processing emotions, becomes increasingly active
during REM sleep.

28
Effects of Sleep Deprivation
In a nutshell, sleep deprivation is caused by consistent lack of sleep or reduced quality of sleep. Getting less
than 7 hours of sleep on a regular basis can eventually lead to health consequences that affect your entire body. This
may also be caused by an underlying sleep disorder.

Your body needs sleep, just as it needs air and food to function at its best. During sleep, your body heals itself and
restores its chemical balance. Your brain forges new thought connections and helps memory retention.

Without enough sleep, your brain and body systems won’t function normally. It can also dramatically lower your
quality of life.

A review of studies in 2010Trusted Source found that sleeping too little at night increases the risk of early death.

Noticeable signs of sleep deprivation include:

 excessive sleepiness
 frequent yawning
 irritability
 daytime fatigue

Stimulants, such as caffeine, aren’t enough to override your body’s profound need for sleep. In fact, these can make
sleep deprivation worse by making it harder to fall asleep at night.

This, in turn, may lead to a cycle of nighttime insomnia followed by daytime caffeine consumption to combat the
tiredness caused by the lost hours of shut-eye.

Behind the scenes, chronic sleep deprivation can interfere with your body’s internal systems and cause more than
just the initial signs and symptoms listed above.

Sleep Disorders
common sleep disorders:

 Insomnia
 Sleep Apnea
 Narcolepsy
 Restless Legs Syndrome
 and REM Sleep Behavior Disorder.

Insomnia

Insomnia is the term for a difficulty getting to sleep or staying asleep. There are two different types of
insomnia. Transient or short-term insomnia and chronic insomnia.

Sleep Apnea

Obstructive sleep apnea is a serious yet common sleep disorder. Your airway repeatedly becomes blocked,
and you’ll stop breathing. When this occurs, you might make choking noises or will snore loudly. You wake
up as your body and brain are oxygen deprived. You may find this happens once or twice a night. However, it
can happen hundreds of times a night in severe cases.

Narcolepsy

29
Narcolepsy causes you to suddenly fall asleep at any time no matter where you are. Often times, you fall
asleep uncontrollably during unusual circumstances, such as while eating. People with narcolepsy are unable
to regulate their sleep-wake cycle.

Restless Legs Syndrome

Restless Legs Syndrome (RLS) presents as an uncontrollable urge or desire to maneuver your legs while
you’re resting. You could also experience unpleasant aching, tingling, burning, and a feeling that something is
crawling in your calves. Sometimes you feel these uncomfortable sensations in other body parts.

REM Sleep Behavior Disorder

When you have REM sleep behavior disorder, you act out your dreams while you sleep. You lack the muscle paralysis
most people experience while asleep. When the condition causes danger to you or anyone around you, it’s taken
particularly seriously

Effects of Long-Term Sleep Reduction


10 Effects of Long-Term Sleep Deprivation

1. Hypertension
2. Heart Attack & Stroke
3. Weight Gain & Obesity
4. Diabetes
5. Depression & Anxiety
6. Faulty Brain Function
7. Memory Loss
8. Immune System Deficiency
9. Decreased Fertility
10. Psychiatric Disorders

Hypertension

Getting less than 5 to 6 hours of sleep per night has been linked to an elevated instance
of hypertension. Because sleep helps our bodies regulate hormones that cause stress, a lack of rest can
amplify the effects of stress on the body. Long-term sleep deprivation has been associated with increased
blood pressure, higher heart rate and inflammation. All of this puts unnecessary strain on your heart.

Heart Attack & Stroke

Sleep deficiency causes a greater instance of fatal cardiovascular problems, such as heart attacks and stroke.
Doctors and researchers believe this is because the lack of sleep may disrupt the parts of the brain which
control the circulatory system or cause inflammation that makes the development of a blood clot more
likely.

Weight Gain & Obesity

The effects of continual sleep problems include rapid weight gain. A lack of sleep is related to higher amounts
of cortisol, a stress hormone; the resulting anxiety, stress and frustration often contribute to emotional
eating and poor nutritional habits. Another hormone, called ghrelin, is produced in the stomach and has
been associated with sleep long-term deprivation; an excess of ghrelin can actually make people feel more
hungry.

Over time, sleep deprivation negatively impacts the body’s metabolism and eating habits. Tiredness often
leads to unhealthy cravings and overindulgence, accompanied by a decrease in stamina and physical activity.
Research has shown that people who feel unrested are more likely to choose foods that are rich in
carbohydrates and sugar.
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Diabetes

Getting as much as 5 hours of sleep at night is still not enough. Research has shown that sleep deprivation
may disrupt the body’s method for processing glucose which cells use for fuel and the amount of insulin that
the body produces. This is why it’s considered a significant risk factor in the development of type 2 diabetes.

Depression & Anxiety

Most people feel irritable if they haven’t had a good night’s sleep, but long-term sleep deprivation has been
linked clinical depression and a more general loss of motivation. Contrarily, patients with depression often
have irregular sleep schedules. Sleep cycles and mood regulation are both regulated by the hormone
melatonin. In fact, lower levels of melatonin are often found in people suffering from depression and those
affected by insomnia.

Anxiety and panic attacks can also be a common reaction for people struggling with chronic sleep deficiency;
they’ve have shown to have a lower tolerance for even mild daily stressors. Like depression, sometimes it
can be difficult to understand what came first: anxiety or the sleep disorder.

Faulty Brain Function

After just one unrestful night, we have all experienced mental fog, fatigue, short temper and lack of focus.
When the brain is not able to rest enough over a longer period of time, mental faculties can decrease
drastically. We know that adequate sleep is necessary for people to feel sharp, concentrate and learn, but it
also impacts our problem-solving skills and the ability to regulate our emotions and make decisions. Sleep
deprived people also have problems with balance, reflexes and motor skills; as a result, they are much more
likely to injure themselves. Drowsiness is a major factor in car accidents.

Memory Loss

Many scientists believe that sleep is important for giving the brain time to organize itself and, specifically, to
commit information from the short-term memory to the long-term memory. Adequate sleep is crucial for
memory recall. Studies show improvement in memory loss after just one night of restful sleep.

Immune System Deficiency

Like the rest of our body, the immune system performs best when we get adequate sleep. A prolonged lack
of sleep causes a similar reaction to high levels of stress; it can decrease your antibody response and make
you more vulnerable when you’re exposed to viruses, even the common cold and flu.

Decreased Fertility

Not only can sleep disorders lower libido, they can have a devastating impact on anyone trying to conceive –
both men and women. The same part of the brain that controls circadian rhythms also regulates the release
of reproductive hormones. Regularly getting fewer than 7 hours of sleep can lead to lower levels of
testosterone and the hormones which trigger ovulation, making conception even more difficult.

Psychiatric Disorders

An extreme and long-term lack of sleep can lead to a number of psychiatric disturbances. Some people
suffering from extended periods of sleep deprivation have experienced symptoms including disorientation,
paranoia and hallucinations. These types of symptoms can sometimes be confused or associated with
schizophrenia.

Drugs that Affect Sleep


1. Alpha-blockers
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Why they're prescribed: Alpha-blockers are used to treat a variety of conditions, including high blood
pressure (hypertension), benign prostatic hyperplasia (BPH) and Raynaud's disease. These drugs relax certain
muscles and help keep small blood vessels open. By keeping the hormone norepinephrine (noradrenaline)
from tightening the muscles in the walls of smaller arteries and veins, they improve blood flow and lower
blood pressure. Because alpha-blockers also relax other muscles throughout the body, they can help improve
urine flow in older men with prostate problems.

Examples: alfuzosin (Uroxatral), doxazosin (Cardura), prazosin (Minipress), silodosin (Rapaflo), terazosin
(Hytrin) and tamsulosin (Flomax).

How they can cause insomnia: Alpha-blockers are linked to decreased REM (rapid eye movement) sleep —
the stage of sleep when people dream — and daytime sedation or sleepiness. The proportion of REM sleep
drops markedly in old age, and people deprived of REM sleep can experience memory problems.

Alternatives: For older people, benzothiazepine calcium channel blockers, another form of blood pressure
medication, are often safer and more effective than alpha-blockers. If the alpha-blocker has been prescribed
to treat BPH, talk with your doctor about the possibility of switching to a 5-alpha-reductase inhibitor such as
dutasteride (Avodart) or finasteride (Proscar), which are safer and generally better tolerated by older
patients.

2. Beta-blockers

Why they're prescribed: Beta-blockers are typically prescribed to treat hypertension (high blood pressure)
and arrhythmias (abnormal heart rhythms). These drugs slow the heart rate and lower blood pressure by
blocking the effect of the hormone adrenaline. Beta-blockers are also used to treat angina, migraines,
tremors and, in eyedrop form, certain kinds of glaucoma.

Examples: atenolol (Tenormin), carvedilol (Coreg), metoprolol (Lopressor, Toprol), propranolol (Inderal),
sotalol (Betapace), timolol (Timoptic) and some other drugs whose chemical names end with "-olol."

How they can cause insomnia: Beta-blockers have long been associated with sleep disturbances, including
awakenings at night and nightmares. They are thought to do this by inhibiting the nighttime secretion of
melatonin, a hormone involved in regulating both sleep and the body's circadian clock. Low levels of
melatonin have sometimes been observed in chronic insomnia.

Alternatives: For older people, benzothiazepine calcium channel blockers, another form of blood pressure
medication, are often safer and more effective than beta-blockers.

A nightly dose of melatonin may also help. A small study published in the journal Sleep in 2012 found that
patients on beta-blockers who also took melatonin fell asleep sooner, had more restful sleep, and slept
longer — an extra 36 minutes a night, on average — than patients taking an inactive placebo. (This was
determined with polysomnography, an overnight sleep test that records brain waves, muscle tone, heart rate
and eye movements.)

3. Corticosteroids

Why they're prescribed: Corticosteroids are used to treat inflammation of the blood vessels and muscles as
well as rheumatoid arthritis, lupus, Sjögren's syndrome, gout and allergic reactions.

Examples: cortisone, methylprednisolone (Medrol), prednisone (sold under many brand names, such as
Deltasone and Sterapred) and triamcinolone.

Examples: cortisone, methylprednisolone (Medrol), prednisone (sold under many brand names, such as
Deltasone and Sterapred) and triamcinolone.

How they can cause insomnia: People often ask why a drug that reduces inflammation would keep them
awake. The answer lies in the adrenal glands, which are responsible for regulating the body's fight-or-flight
response. Too much stress can keep the body awake and the mind stimulated by exhausting the adrenal

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glands; corticosteroids can do the same thing, wreaking havoc on all the systems that allow you to relax and
sleep, causing insomnia and unpleasant dreams.

Alternatives: Ask your doctor or pharmacist whether you can take your medication in a single dose early in
the day.

4. SSRI antidepressants

Why they're prescribed: SSRIs (selective serotonin-reuptake inhibitors) are used to treat symptoms of
moderate to severe depression. SSRIs block the reabsorption (reuptake) of the neurotransmitter serotonin in
the brain, which may help brain cells send and receive chemical messages, easing depression. They're called
selective because they seem to primarily affect serotonin, not other neurotransmitters.

Examples: citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox),
paroxetine (Paxil, Pexeva) and sertraline (Zoloft).

How they can cause insomnia: Just as it isn't known exactly how SSRIs work, it isn't known exactly how these
drugs interfere with sleep. Studies have shown, however, that SSRIs cause agitation, insomnia, mild tremor
and impulsivity in 10 percent to 20 percent of the people who take them.

Although about half of people who take SSRIs say that the drugs make them feel better, many continue to
struggle with symptoms that can make life miserable, especially insomnia. We know this from researchers at
the University of Texas Southwestern Medical Center in Dallas, who combed through data from the STAR*D
trial, the largest and longest study ever done on depression treatment, and published their findings in 2011.
Almost all of the subjects in the Star*D trial, which was funded by the National Institute of Mental Health,
said they continued to have problems with insomnia, with 81 percent reporting being unable to sleep in the
middle of the night.

Alternatives: If you are experiencing anxiety or insomnia while on an SSRI (or any other antidepressant, for
that matter), it's important to tell your prescribing doctor right away. Sleeplessness — in itself a marker of
depression — can make you even more depressed.

Because antidepressants vary in their side effects, a change in dosage or switching to another medication
may help you feel better without causing insomnia or other sleep disturbances. A selective
serotonin/norepinephrine reuptake inhibitor (SSRI/SNRI), a newer-generation antidepressant, offers some
advantages in improving relaxation and sleep. Of the three drugs in this category
(clomipramine, duloxetine and venlafaxine), I find venlafaxine to have the least adverse side effects in older
patients and to be easier to dose to a therapeutic level.

Many people find that cognitive behavior therapy works just as well as medication. (Cognitive therapy aims
to help people overcome their difficulties by changing their thinking, behavior and emotional responses.)
Others report success with such approaches as acupuncture, exercise, changes in diet, meditation, relaxation
therapy and the like.

5. ACE inhibitors

Why they're prescribed: Angiotensin-converting enzyme (ACE) inhibitors are used to treat high blood
pressure, congestive heart failure and other conditions. These drugs help relax blood vessels by preventing
the body from producing angiotensin II, a hormone that causes blood vessels to narrow and, in turn, blood
pressure to rise.

Examples of ACE inhibitors include: benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), fosinopril
(Monopril), lisinopril (Prinivil, Zestril), moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril
(Altace) and trandolapril (Mavik).

How they can cause insomnia: ACE inhibitors boost the body's levels of bradykinin, a peptide that enlarges
blood vessels. Bradykinin is thought to be the cause of the hacking, dry cough that up to a third of all patients
who take an ACE inhibitor develop. This chronic, round-the-clock cough can be severe enough to keep
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anyone awake. ACE inhibitors can also cause potassium to build up in the body (another type of electrolyte
imbalance) and lead to diarrhea, as well as leg cramps and achy joints, bones and muscles — all of which can
disturb normal sleep.

Alternatives: If you're taking an ACE inhibitor for a cardiovascular problem, talk with your doctor or
pharmacist about possibly switching to a benzothiazepine calcium channel blocker, another form of blood-
pressure medication that is often better tolerated by older adults. This is especially important for African
Americans and Asian Americans, who, because of differences in their renin-angiotensin systems, have much
higher incidences of adverse side effects.

If your condition is accompanied by fluid retention, your doctor may consider adding a low dose of a long-
acting loop diuretic, such as torsemide.

6. Angiotensin II-receptor blockers (ARBs)

Why they're prescribed: ARBs are often used to treat coronary artery disease or heart failure in patients who
can't tolerate ACE inhibitors or who have type 2 diabetes or kidney disease from diabetes. Instead of
blocking the body's production of angiotensin II, ARBs prevent it from exerting its blood vessel-constricting
effects.

Examples of ARBs include: candesartan (Atacand), irbesartan (Avapro), losartan (Cozaar), telmisartan
(Micardis) and valsartan (Diovan).

How they can cause insomnia: Like ACE inhibitors, ARBs frequently lead to potassium overload in the body,
causing diarrhea as well as leg cramps and achy joints, bones and muscles — all of which can disturb normal
sleep.

Alternatives: As with ACE inhibitors, I'd recommend you consult with your health care provider about the
advisability of switching to a benzothiazepine calcium channel blocker, which is often better tolerated by
older adults. This is especially important for African Americans and Asian Americans, who because of
differences in their renin-angiotensin systems, have much higher incidences of adverse side effects.

A low dose of a long-acting loop diuretic such as torsemide may also be desirable.

7. Cholinesterase inhibitors

Why they're prescribed: Cholinesterase inhibitors are commonly used to treat memory loss and mental
changes in individuals with Alzheimer's disease and other types of dementia.

Examples: donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon). The main side effects of
these drugs include diarrhea, nausea and sleep disturbances.

How they can cause insomnia: These drugs are thought to work by inhibiting the enzyme in the body that
breaks down acetylcholine (a neurotransmitter that's important for alertness, memory, thought and
judgment) and thus boosting the amount available to brain cells. This, in theory, slows the patient's loss of
memory and helps him or her perform daily activities with fewer problems. But blocking the breakdown of
acetylcholine — which is everywhere in the body, not just in the brain — can interfere with all kinds of
involuntary body processes and movements, including those related to sleep.

In addition to insomnia and abnormal dreams, the identified side effects of cholinesterase inhibitors include
serious changes in heart rhythm, diarrhea, nausea and vomiting as well as leg cramps and muscle spasms —
all of which can interfere with normal sleep patterns.

Alternatives: It's important to remember that cholinesterase inhibitors cannot reverse Alzheimer's disease or
slow the underlying destruction of nerve cells. And because the Alzheimer's-afflicted brain produces less
acetycholine as the disease progresses, all medications in this class eventually lose whatever effectiveness
they may be presumed to have.

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For these reasons, it may be worthwhile to talk with your doctor (or the doctor treating your loved one)
about whether the adverse effects of the drug prescribed outweigh its possible benefits. In my experience,
that's nearly always the case.

8. Second-generation (nonsedating) H1 antagonists

Why they're prescribed: H1 antagonists, which are in a class of drugs commonly known as antihistamines,
inhibit the body's production of histamine — the chemical that's released when you have an allergic reaction.
Elevated histamine levels cause such common allergic reaction symptoms as itching, sneezing, runny nose,
watery eyes, nasal congestion and hives.

Second-generation H1 antagonists, also known as nonsedating antihistamines, do not have the same side
effects as first-generation antihistamines, such as diphenhydramine (Benadryl), which suppress the central
nervous system, causing severe drowsiness.

Examples of second-generation H1 antagonists include: azelastine (Astelin) nasal spray, cetirizine (Zyrtec),
desloratadine (Clarinex), fexofenadine (Allegra), levocetirizine (Xyzal) and loratadine (Claritin).

How they can cause insomnia: In varying degrees, all H1 antagonists block acetylcholine, a nervous system
neurotransmitter, and thus can cause anxiety and insomnia.

Alternatives: Since these second-generation antihistamines are typically active in the body for around eight
hours, you may find that taking your daily dose in the morning may be all that's needed to resolve any sleep-
related problems it may be causing.

9. Glucosamine and chondroitin

Why they're used: Glucosamine and chondroitin are dietary supplements that are used to relieve joint pain,
improve joint function and lessen inflammation. (Both are found naturally in the human body.) Many
arthritis supplements contain glucosamine and chondroitin, both of which are regulated by the Food and
Drug Administration as a food rather than a drug.

How they can cause insomnia: Researchers aren't sure exactly how glucosamine and chondroitin work, but
studies identify a range of gastrointestinal side effects, including nausea and diarrhea, as well
as headaches and insomnia.

Alternatives: While many people take glucosamine and chondroitin, alone or together, for osteoarthritis,
they may not help at all. A recent analysis of many studies of these supplements failed to find evidence that
they slow joint destruction or relieve pain.

A 2010 survey of Consumer Reports subscribers found that among those who identified osteoarthritis as one
of their most bothersome conditions, yoga and massage were rated twice as helpful as glucosamine and
chondroitin.

If you choose to use one or both of these supplements, you should be aware that glucosamine has a longer
half-life (the time it's active in the body) than chondroitin. So if glucosamine is part of your medication
regimen, taking your daily dose in the morning should prevent problems with insomnia.

You may also wish to consider asking your doctor for a prescription of tramadol 50mg tablets and taking one
with an acetaminophen 325mg tablet two to three times a day. This should work well to relieve pain.

10. Statins

Why they're prescribed: Statins are used to treat high cholesterol.

The top-selling statins are atorvastatin (Lipitor), lovastatin (Mevacor), rosuvastatin (Crestor) and simvastatin
(Zocor).

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How they can cause insomnia: The most common side effect of all types of statins is muscle pain, which can
keep people who take them awake at night and unable to rest. In the worst cases, the pain caused by statins
can be immobilizing.

Studies show that statins can interfere with muscle growth by inhibiting the production of satellite cells in
the muscle. Muscle weakness and aches throughout the body can be symptoms of statin-
induced rhabdomyolysis, a breakdown of skeletal muscle that causes muscle fibers to be released into the
bloodstream, sometimes harming the kidneys.

Researchers have found that fat-soluble statins — which include Lipitor, Mevacor, Vytorin and Zocor — are
more likely to cause insomnia or nightmares because they can more easily penetrate cell membranes and
make their way across the blood-brain barrier, which protects the brain from chemicals in the blood.

Alternatives: If you're among the millions of older Americans who haven't been diagnosed with heart disease
but are taking these drugs to lower your slightly elevated cholesterol, ask your doctor or other health care
provider about making changes to your diet and getting regular exercise instead of using statins. You also
might try lowering your blood levels of homocysteine — which is linked to high cholesterol — by taking a
combination of sublingual (under-the-tongue) vitamin B12 (1,000 mcg daily), folic acid (800 mcg daily)
and vitamin B6 (200 mg daily).

V. Materials/Devices:

1. Laptop
2. Mobile Phone

V1. Teaching Methodologies:

Lecture/Discussion

Power Point Presentations

Group Reporting

Sharing Information

V11. Assessment:

Quiz

Graded recitation

V111. Activity:

Prepare a circadian preference

Resources:

Pinel, John P. (2011), Inc., Biopsychology, 8th ed,. Pearson, Education, Inc.,

Garrett, Bob & Hough, Gerald (2021) Brain and Behavior: An Introduction to Behavioral
Neuroscience. Sage Publications, Inc.,
https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Understanding-Sleep?
fbclid=IwAR1dHzMaDTTqAfMVaSEzvgVK0Jny7bz3I3_RSbeLSxkXKsA4yzjPOf4H1gM

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Module 5

This module touches the role of the nervous system in reproductive behavior.

I. Learning Outcomes:

At the end of the topic, the students should be able to:

1. Discuss the stages of neuro development.


2. Explain the postnatal cerebral development of human infants.
3. Summarize the brain development in the first year of life and the importance of early childhood
experiences for brain development.

II. Topic 5. Neural Development


5.1 Stages of Neuro Development
5.2 Postnatal Cerebral Development of Human Infants
5.3 Brain Development in the First Year of Life
5.3 The Importance of Early Childhood Experiences for Brain Development.

III. Time Frame: Week 7-8

Discussion:

Stages of Neuro Development


Neuronal Development

There are four stages recognized in the process of neuron development and the formation of the nervous system.

Throughout these formative stages, all cells which form the basis of every organ and system that come together to
ultimately develop into the sentient creature that you are, are formed and assigned to their lifelong destinations and
physiological roles.

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Stage 1: Neurogenesis

This is the very first stage of the foundational process of neuronal development. During this stage, cells that have yet
to be differentiated will undergo mitosis to produce either stem cells, or neuroblasts, which will ultimately be
differentiated into many different types of neurons.

The neuroblasts and stem cells can be thought of as essentially the same things. They are, functionally, precursors to
what eventually becomes a neuron.

The main difference is that neuroblasts are the stars of the show when it comes to embryonic development, whereas
stem cells have a stronger presence in adult neurogenesis (development of neurons takes place throughout the
entire lifetime).

These cells continue dividing until they eventually form what is called the “ventricular zone,” which is a densely-
packed layer of… well, cells! This ultimately leads to the formation of three separate zones : the ventricular zone,
intermediate zone, and the marginal zone.

The neurons and glial cells are formed in the intermediate zone.

Stage 2: Cell Migration

Here is where things start to get even more exciting and take on a bit more complexity. In this stage, cells that were
previously responsible for creating the ventricular zone now must move great distances to establish distinct cell
populations for further embryonic development.

These migrations are genetically pre-determined and so are not random in any way.
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Keep in mind that the formation of the ventricular, intermediate, marginal zone is due to the movement of cells. So,
even though the formal process of migration has not officially begun, this is the mechanism behind the formation of
these zones.

Further, cells in the intermediate zone have already begun developing into neural and glial cells. (But these are not as
special as the ones coming up.)

What constitutes cell migration is the movement of more cells (which are being formed during the ongoing process
of neurogenesis) along the radial glia toward the marginal zone from the ventricular zone. Once they reach the
marginal zone, they begin differentiation.

Stage 3: Differentiation

Now, the process of differentiation is different from normal cell mitosis in that the embryo’s DNA (Deoxyribonucleic
Acid) dictates the nerve cells’ specific physiology for their future core functions. Here is where it is determined what
type of nerve cell they will become.

This process continues on, hand-in-hand, with Stage 4.

Stage 4: Outgrowth

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In this stage, the foundational cells of the nervous system truly begin to take the shape.

Here is where the axons and dendrites begin to form – differentiation continues through this stage to direct these
developments, as each neuron requires a distinct physicality based on their ultimate function.

The proliferation of synapses – the junction between nerve cells which allows for communication throughout the
entirety of the nervous system – begins here as well. The synapses, axons, and dendrites all work together to create
this system of communication: Dendrites receive information from a given stimulus, pass it through the axon and to
the synapse, which then transfers that information to another neuron until all information ends up in your brain.

Going back to differentiation: As previously noted, there are many – many – different types of neurons. What the
developing neurons will become is not only determined by DNA expression, but also by the location of the cell during
development and relative position to neighboring nerve cells.

Postnatal Cerebral Development of Human Infants


While babies come into the world with some very useful survival reflexes, they are still strikingly helpless, in large
part because the cerebral cortex is still quite immature.

As the highest, most recently evolved part of the brain, the cerebral cortex is responsible for all of our conscious
thoughts, feelings, memories, and voluntary actions.

Although all of the neurons in the cortex are produced before birth, they are poorly connected. In contrast to the
brain stem and spinal cord, the cerebral cortex produces most of its synaptic connections after birth, in a massive
burst of synapse formation known as the exuberant period. At its peak, the cerebral cortex creates an astonishing
two million new synapses every second. With these new connections come a baby’s many mental milestones, such
as color vision, a pincer grasp, or a strong attachment to his parents.

By two years of age, a toddler’s cerebral cortex contains well over a hundred trillion synapses. This period of synaptic
exuberance varies in different parts of the cerebral cortex: it begins earlier in primary sensory regions, like the visual
cortex or primary touch area of the cortex, while it takes off somewhat later in the temporal and frontal lobes, brain
areas involved in higher cognitive and emotional functions. Nonetheless, the number of synapses remains at this
peak, over-abundant level in all areas of the cerebral cortex throughout middle childhood (4-8 years of age).
Beginning in the middle elementary school years and continuing until the end of adolescence, the number of
synapses then gradually declines down to adult levels.

This pattern of synaptic production and pruning corresponds remarkably well to children’s overall brain activity
during development. Neuroscientists have found dramatic changes in the level of energy use by children’s brains
over the first several years of life—from very low at birth, to a rapid rise and over-shoot between infancy and the
early elementary school years, followed by a gradual decline to adult levels between middle childhood and the end
of adolescence. In other words, children’s brains are working very hard, especially during the period of synaptic
exuberance that corresponds to the various critical periods in their mental development.

Besides synapse formation and pruning, the other most significant event in postnatal brain development is
myelination. Newborns’ brains contain very little myelin, the dense impermeable substance that covers the length of
mature brain cells and is necessary for clear, efficient electrical transmission. This lack of myelin is the main reason
why babies and young children process information so much more slowly than adults—why it might take a toddler a
minute or more to begin responding to a request such as “Joey, bring Mommy the teddy bear.” Myelination of the
cerebral cortex begins in the primary motor and sensory areas—regions that receive the first input from the eyes,
ears, nose, skin, and mouth—and then progresses to “higher-order,” or association regions that control the more
complex integration of perception, thoughts, memories, and feelings. Myelination is a very extended process:
although most areas of the brain begin adding this critical insulation within the first two years of life, some of the
more complex areas in the frontal and temporal lobes continue the process throughout childhood and perhaps well
into a person’s 20s. Unlike synaptic pruning, myelination appears to be largely “hard-wired.” Its sequence is very
predictable in all healthy children, and the only environmental factor known to influence it is severe malnutrition.

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Brain Development in the First Year of Life

First Year, 0-12 Months


During the first year of a child’s life, his brain will double in size. Much of this growth occurs in a part of the
brain called the cerebellum, which is in charge of physical development and motor skills. This development
helps babies learn to control their bodies and movement. They learn to hold up their heads, to roll over,
grasp objects, and even to stand up. Meanwhile, the visual cortex, the part of the brain that helps us see,
changes rapidly, and the baby starts to recognize faces. Next, the limbic structure, the part of the brain that
controls emotion and long-term memory, begins to develop, helping the baby become more aware of the
world around him.

Signs of Healthy Development *

 Baby loves to look into your face. He tries to mimic your expressions, and loves to play peek-a-boo.
 He has a healthy appetite, and is growing between well-baby visits.
 He responds to familiar faces.
 He starts to babble and to make a range of impressive sounds.
 He starts to lift his head, to roll over, to crawl, and – closer to the end of the first year, pulls himself
to a standing position.
Language And Literacy

Children are learning about language even during the first few months of life. Newborns use body
language, sounds, and facial expressions to express their wants and needs.

What You Can Do to Help:

 Talk softly to your baby in a calm and soothing voice using normal speech and words.
 Respond to your baby’s sounds.
 Show delight when she coos and babbles.
 Use your baby’s name when you speak.
 Your baby’s crying tells you she needs something.
Thinking Skills

During his first year, the baby is starting to learn about important ideas like cause and effect. He is also
developing a sense of safety and security.

What You Can Do to Help:

 Infants and toddlers learn through play. When your baby drops your keys, for example, she wants
to see how you will respond.
 Play along with her to encourage her to explore and learn.
 Be very patient and have a sense of humor when playing with your baby.

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Self Control

Newborns have very little, if any, self-control. It is natural for infants to fuss when they are frustrated. Their
tantrums and cries just reflect their developmental stage, not that they are spoiled.

Babies use crying as a way to let parents know that they need something. Your baby needs you to show
your calm love and support.

What You Can Do to Help:

 To encourage her self-control, it is helpful for you to stay calm and to show her how to act.
 Your child won’t be the first (or last) to cry at the grocery store, restaurant, or other very public
place. Remain calm, try to sooth her, and walk outside with her if you have to.
 Babies thrive on routine. When she can count on regular naptimes, cuddling, diaper changes and
feedings, her level of self-control will begin to develop.
Self Confidence

Newborns begin to develop self-confidence when they feel loved and safe.

What You Can Do to Help:

 Comfort your baby when she cries and respond to her needs.
 Make her feel loved by holding her close and speaking softly to her.
 Cheer for her and smile at her as often as possible. Let her know that she is adored.

The Importance of Early Childhood experiences for Brain Development

Children are born ready to learn, and have many skills to learn over many years. They depend on parents,
family members, and other caregivers as their first teachers to develop the right skills to become
independent and lead healthy and successful lives. How the brain grows is strongly affected by the child’s
experiences with other people and the world. Nurturing care for the mind is critical for brain growth.
Children grow and learn best in a safe environment where they are protected from neglect and
from extreme or chronic stress external icon with plenty of opportunities to play and explore.
Parents and other caregivers can support healthy brain growth by speaking to, playing with, and caring for
their child. Children learn best when parents take turns when talking and playing, and build on their child’s
skills and interests. Nurturing a child by understanding their needs and responding sensitively helps to
protect children’s brains from stress. Speaking with children and exposing them to books, stories, and
songs helps strengthen children’s language and communication, which puts them on a path towards
learning and succeeding in school.

Exposure to stress and trauma can have long-term negative consequences for the child’s brain, whereas
talking, reading, and playing can stimulate brain growth. Ensuring that parents, caregivers, and early
childhood care providers have the resources and skills to provide safe, stable, nurturing, and stimulating
care is an important public health goal.

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When children are at risk, tracking children’s development and making sure they reach developmental
milestones can help ensure that any problems are detected early and children can receive the intervention
they may need.

Learn more about supporting early childhood experiences:

 Tracking developmental milestones


 Preventing abuse and neglect
 Positive parenting tips
 Healthy childcare external icon
A healthy start for the brain
To learn and grow appropriately, a baby’s brain has to be healthy and protected from diseases and other
risks. Promoting the development of a healthy brain can start even before pregnancy. For example,
a healthy diet and the right nutrients like sufficient folic acid will promote a healthy pregnancy and a
healthy nervous system in the growing baby. Vaccinations can protect pregnant women from
infections that can harm the brain of the unborn baby.

During pregnancy, the brain can be affected by many types of risks, such as by infectious diseases
like Cytomegalovirus or Zika virus, by exposure to toxins, including from smoking or alcohol, or when
pregnant mothers experience stress, trauma, or mental health conditions like depression. Regular health
care during pregnancy can help prevent complications, including premature birth, which can affect the
baby’s brain. Newborn screening can detect conditions that are potentially dangerous to the child’s brain,
like phenylketonuria (PKU). external icon
Healthy brain growth in infancy continues to depend on the right care and nutrition. Because children’s
brains are still growing, they are especially vulnerable to traumatic head injuries, infections, or toxins, such
as lead. Childhood vaccines, such as the measles vaccine, can protect children from dangerous
complications like swelling of the brain. Ensuring that parents and caregivers have access to healthy foods
and places to live and play that are healthy and safe for their child can help them provide more nurturing
care.

V. Materials/Devices:

3. Laptop
4. Mobile Phone

V1. Teaching Methodologies:

Lecture/Discussion

Power Point Presentations

Group reporting

Short Video

V11. Assessment:

Quiz

V111. Activity:
43
Explain the following questions :

 Which of the developmental changes occurs in the brain after birth?


 What are the most important changes of the brain after birth?

Resources:

Pinel, John P. (2011), Inc., Biopsychology, 8th ed,. Pearson, Education, Inc.,

Ziehen, Theodor (2008), Introduction to Physiologi`cal Psychology. Kessinger publishing.,

https://brainmadesimple.com/neuronal-development/?
fbclid=IwAR2kE1gZbqJzHa0Ld3GHjmLawnysPoN8w_06crxTq7rmowvgCpU9z9dxu-Y
http://www.urbanchildinstitute.org/why-0-3/parenting/guide/first-year?
fbclid=IwAR0CuBETKE0LjXBSknLwD2f3K0H1rRFcmuWYgLOh5xObD8u0ATI2DGC0X1s
https://www.zerotothree.org/resources/1379-what-are-the-most-important-changes-in-
the-brain-after-birth?fbclid=IwAR04iQDL52F-
4x7hgJsSvXT3rwwXEZqE5UT8PlBCr6WLzxIa7KISljf54O4

MIDTERM EXAMINATION
Week 9

44

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