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Nervous

The document provides an overview of the coordination in A2 Biology, focusing on the structure and function of nerve cells, types of neurones, and the process of action potentials. It explains the roles of sensory, motor, and relay neurones, as well as the mechanisms of resting potential, depolarisation, repolarisation, and hyperpolarisation. Additionally, it discusses the all-or-nothing law of nerve impulses and the significance of the refractory period in action potential propagation.

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0% found this document useful (0 votes)
28 views46 pages

Nervous

The document provides an overview of the coordination in A2 Biology, focusing on the structure and function of nerve cells, types of neurones, and the process of action potentials. It explains the roles of sensory, motor, and relay neurones, as well as the mechanisms of resting potential, depolarisation, repolarisation, and hyperpolarisation. Additionally, it discusses the all-or-nothing law of nerve impulses and the significance of the refractory period in action potential propagation.

Uploaded by

johnmrg990
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Coordination

A2 Biology ( 9700)
2022-2023
CNS …..brain and spinal cord
Nerves attached to brain …..cranial nerves
Nerves attached to spinal cord …spinal nerves

a Slower ummuFaster
Structure of nerve cells / neurones

Contain nucleus , many mitochondria , large amount of RER ( grouped together ) forming Nissl’s
Cell body granules …..associated for production of proteins and neurotransmitters

Dendrone Extension from cell body sub divided into dendtrites carry nerve impulses towards cell body .

Axon
Long fibre carrying nerve impulses away from the cell body

Schwann cells It provides insulation to axon , they wrap themselves around the axon where the layers of their
membrane build up around axon forming myelin sheath

Nodes of The space between adjacent Schwann cells lacking myelin sheath …( size is around 2-3
Ranvier um …occurs every 1-3 mm in neurones of human )
Types of neurones

Sensory neurone
Cell body with nucleus. And many mitochondria and RER , short axon , one long dendrone ( afferent axon ) ,
Schwann cells, myelin sheath , Nodes Of Ranvier , with cell body in swelling of a spinal cord called ganglion

Motor neurone

Cell body with nucleus. And many mitochondria and RER , many dentrites , long axon , Schwann cells, myelin sheath ,
nodes Of Ranvier ( dendrites attached to cell body , nissl’s granules , axon terminals , cell body in CNS.

Relay neurone Have short dendrites (extensions ) , found entirely in the CNS , NO Schwann cells, no nodes of Ranvier ,
cell body with mitochondria , nucleus , RER
Sensory receptors Respond to stimulus
Act as transducers , convert stimulus into electrical energy / impulse
Generate action potential
Dorsal root ganglion
Reflex arc

Spinal reflex like hand withdrawal :


1. Stimulus …..heat object detected by SENSORY RECEPTORS
2. Receptors …if the temperature receptors detect temperature above THRESHOLD VALUE ….so this will generate
an ACTION POTENTIAL .
3. Sensory neurones ..action potential pass along the sensory neurone to spinal cord .
4. Relay neurone ( grey matter of spinal cord ) link the sensory to motor neurone via Synapse .
5. Motor neurone carry action potential away from spinal cord to the effector ( biceps muscles of the forearm )
6. Muscle contract …bring a response which is raising up the hand away from the hot object
Types of transporter in cell surface membrane of axon

Resting Chemical gradient


Resting
Passive movement ( no ATP )
Active movement ( needs ATP )
Electricalgradient 1 Ion ( K+ / Na+ ) leak channels
Sodium potassium pump acts continuously
to transport ions ( sodium and potassium
across the membrane ) Na+ out and
potassium pumped in K+

Always open , movement of ions by


facilitated diffusion …allowing movement of
sodium ions and potassium ions across the
membrane down their chemical gradient ( i.e
concentration gradient )

2 Voltage gated channels


Action
Alternate between being open
and closed …respond to the
changes in the potential difference
across the membrane .
Resting potential https://youtu.be/7NY6XdPBhxo
100+
30+

I.e 70 less=-70 m volts Polarised

1. Sodium potassium pump , sodium actively 1. The membrane of the neurone is more
transported outside the axon and potassium inside … permeable to potassium ions , through having
for every 3 Na+ ions pumped out , 2 K+ ions move more potassium leak channels than Na+ ion
in …so becoming more positive outside ( creating a leak channels ….K+ diffuse will diffuse out and
negative resting potential + change ions sodium ions will diffuse in down chemical
concentration inside and outside the cell) gradient.
2. Where the axon membrane is 100 more times
permeable to K+ ions ..causing further in
crease in potential difference between negative
inside and positive outside axon

2.we have high K+ ion concentration inside the


cell , and high Na+ ion concentration outside Se we need energy to maintain the negative
( building chemical gradient ) resting potential (-70 millivolts )situation
4. Organic anions ( proteins ) contribute to the negative resting potential of neurones

Why resting potential requires energy

Sodium potassium pump …..sodium ions are pumped actively out of the axon while potassium ions
are actively pumped inside by sodium potassium pump
Against their concentration gradient
31/7/2023
Part 2
Action potential
Action potential

Threshold potential is the potential difference across the membrane above which the an impulse is sent along a
neurone -

SomU.
+ + + Potential difference across the
Polarisation …..resting potential
+
+
++++t
. . . . .
membrane = -70 mvolts

Deploristaion … changing the potential difference across the


membrane so it becomes less negatively charged inside ( +ve
inside and -ve outside ) above Tomu
- ... (-30, -10,+20 --.)

Hyper polarisation : a decrease in the potential difference


across the membrane by becoming more negatively charged
inside below zumu.... (-80, -90...--(

Resting Action potential

Ion voltage gated channels


Sodium potassium pump Ion leak channels
K+ / Na+

Energy Open Potential difference


ElectroChemical gradient
7. The K+ voltage gated channels
1. Resting potential ….polarised …leak 4. Once the action potential reaches
close , sodium potassium pump cause
channels of Na+ and K+ions are open , around +40 millivolts inside the axon
sodium ions pumped outand
where DEPOLARisation has occured
Voltage gated channels of K+ and Na+ potassium ions inside .. returning to
resting potential …at this point voltage gated sodium ions
are closed …-70 mv
will close and the potassium volatage
gated channels open .
2. The stimulus exceeds the threshold ,
voltage gated sodium channels open
….sodium diffuse in through these
channels along electrochemical gradient DrDa
Dr
K+ volatge gated
channels closed

5.repolarisation , where with some K+


voltage gated channels =now open ..this
-55
7 will cause the other voltage gates of K+
K+ volatge gated channels begin to open ..and more K+
channels closed
outflux .

This will reverse the potential difference


3. More sodium voltage gated
across the membrane and become channels open , causing a greater
6. The outward movement of K+ions
and the Slightly delay of the closing of
DEPOLARISED … influx of sodium ions …positive feed
potassiun volatge gated channels cause
VOLTAGE GATED K+ is still back mechanism increasing
temporary OVERSHOOT of electrical
CLOSED depolarisation amplitude gradient , with the axon inside becoming

88D
more negative than outside , this is
.......

(()()() called HYPERPOLARISATION

+ K+ volatge gated
channels closed
efflux.
k*
Nat '

888
+
44 I

(08"
t

. - I - ++
+ t +

= - - -

Na+ VG K+ VG I

+
++ ++++ +
Na+ VG K+ VG
-...........
- - - - - -

t -------
+ ++ ++
Resting potential
+ ++++
x +++
t
+
+
+

Action potential
Polarised Repolaisation Hyperpolyrisation
Depolarises
-70 mV -55mV ….+40mv

A B
Resetting after hyperpolarisation : Read only

: The voltage gated potassium channels close , sodium potassium pump casue sodium pumped out and
potassium in …for every 3 Na+ ion pumped out , 2 K+ ions move in ..so becoming more positive outside
….then Electrical gradient will pull potassium back into the nerve cell /axon
Decreasing the positive charge from outside
returning the resting potential state of the axon which is to be replaorised …..
Action potential

Threshold potential is the potential difference across the membrane above which an impulse is sent
along a neurone .

Depolarisations (.I
' polarisation )a change in the potential difference across the membrane so it

becomes less negatively charges inside ( +ve inside , -ve outside ) Depolarised

Hyper polarisation : a decrease in the potential difference across a membrane by becoming MORE Hyper
negatively charged inside polarised

1. Resting : leak channels of K+ ion are open , volatge gated of


potassium and sodium were closed .
2. Stimulus exceeding threshold, some of the voltage gated sodium ions
open , therefore sodium ios diffuse in through channels along their
electrochemical gradient.
Being positively charged , this will reverse the potential difference across
the ions and become DEPOLARISED …..VOLTAGE GATED
POTASSIUM IS STILL CLOSED .
3. As more sodium ions diffuse into the cell, more voltage gated sodium
ions open , causing a greater influx of sodium ions ….positive feed back
mechanism .
Increasing amplitude of depolarisation .
Action potential only occurs after reaching the threshold( membrane potential inside reaches about -50 millivolts)
4. Once the action potential reaches around +40 millivolts '
inside the axon where DEPOLARisation has occured …at this
point voltage gated sodium ions will close ( deactivated ) and the
potassium volatage gated channels open .

5. REPOLARISATION , where with some K+ voltage gated


channels now open ..this will cause the other voltage gates on
K+ channels begin to open …and more K+outfux ..

6. The outward movement of K+ions and the Slightly delay of


the closing of potassiun volatge gated channels cause temporary
OVERSHOOT of electrical gradient , with the axon inside
becoming more negative than outside , this is called
HYPERPOLARISATION .

7. The gate of potassium close , sodium potassium pump casue


sodium pumped out and potassium in …returning the resting
potential state of the axon which is to be replaorised .
As one region of the axon produces an action
potential and become depolarised ,
it acts as a stimulus for the depolarisation of
the next region of the axon/ membrane . This
reversal of electrical charge is reproduced and -

action potentials are generated along each


small region of the axon membrane .
As one action potential triggers the next , the
Under previous region of the membrane returns to its

stand resting potential i.e its repolarised.


The size of the action potential remains the
same from one end of the axon to the other . Cant be depolarised
Strictly speaking , nothing physically moves ( depolarisation means Na+ voltage gated channels open )
from place to place along the axon of the This is not possible in repolarisation and hyperpolarisation state
neurone , but rather the reversal of electrical Because the sodium voltage gated channels are inactive .
charge is reproduced at different points along
the axon membrane .....like MEXICAN WAVE.

Refractory period :
A period of time following an action potential . When a neurone can’t be stimulate ( peroid of time
Voltage gated channels are inactivated so dont respond to depolrisation )
1) ensure the action potential are separated without merging ….limiting number of action potentials
passing by neuron per unit time ..determine frequency of action potentials
2) allow action potential to travel in one direction
Na+ voltage gated channels are inactive
K+ voltage gated channels are open
Membrane is repolarised then hyperpolarised
Cant be depolarised

Refractory period in english period


during which an organ , cell cant repeat
a particular action . …not ready to
receive another stimulus

Refractory period inactivation of voltage gated sodium channels ..which occurs at the peak of action
potential ( +40 mVolts ) …and persist through most of the overshooting period .
Overshooting describe …….
Refractory period ensure that an action potential will only travel forward down the axon not back
wards
. Resting potential Polarized (-70mv)


1

I
4+ I x t
+

1.Stimulus exceeds the


threshold -50mv
2. Open voltage gated Na+
2
Slight delay in closing of voltage

4 channels .
gated K= ions
-

Na+
+ ++++t +

+
+ + +t t
+ -- - -

Na+ open
Influx K+ open u +
t
-- - +
+
t ++ ↓

A
Efflux

RB
+ +
t+ ++ +
I

-
- ---

K+
Efflux
3
Action potential reaches +40mv inside the axon
…..repolarisation ……voltage gate Na+ close
….potassium voltage gated .channels open
Repolarisation
K+ volatge gated open
Na+ volatge gated inactive

Depolarisation
Na volatge gated open
K+ voltage gated closed
Hyperpolarisation
Still K+ volatge gated open
Resting potential
Na+ voltage inactive
Polarisation
Leak / pump
+

+
+
7 ++
- -

Pump and leak


Understand

Propagation of nerve impulse


Second action
A potential is initiated :

Resting potential
Yet at the site of first
High sodium ion
action potential …
concentration
repolarisation ..K= VG
outside and high
channels open and
potassium ion
K+ ions move out of
concentration
the axon …Na+ VG
inside
Repolarisation
closed …followed by
And

B hyperpolarisation hyperpolarisation
Action potential
D
( depolarisation): Third action potential
Na+ VG channels initiated..by the second
open and K+ VG action potential .
closed , Na+ flow At the site of first
inside into the action potential …K+
axon ..depolarizing & diffuse back into axon
the membrane Resting potential restore the resting
( polarisation)
potential
Resting Resting
P.D= -70 m.v Depolarisation ………repolarisation………hyperpolarisation P.D = -70 m.v

Over shooting
Na+ voltage gated channels Delay in closing of K+ voltage gated channels
Na+ diffuse in More K+ ions leave axon

P.D more negative


K+ voltage gated channels closed
Below -70 m.v
Exceed -55m.v
Till +40 mv Na+ Voltage gated channels inactive
K+ voltage gated channels open
P.D less negative
K+ diffuse out

P.D more negative

Refractory period
Na+ Voltage gated channels inactive
No depolarisation
1/ 8/2023
Part 3
All or nothing law
Myelinated neurone
Synapse
Stimulus …sensory receptors ( transducers ) generate
receptor potential ….if exceeds the threshold ..action
potential in sensory neurone .

All or nothing law

1. Nerve impulses are described as all or nothing responses.


2. There is a certain level of stimulus , which is threshold
3. That triggers the impulse
4. Potential difference is below the threshold , no impulses generated
5. Potential difference above the threshold value , an impulse will be
generated
6. The action potential is the same regardless of how much the stimulus is
above the threshold value .
7. We can determine the size of the stimulus by ;
A) frequency of impulses passing in a unit time , where the larger the
Sensory
stimulus , the more the action potentials that are generated per unit time . Stimulus Receptor exceed

neurone
->
Heshuld

Stimulus
B) number of neurones carrying action potential . e
-
lectrical impulse electical impulse.
-
potential
-

receptor~potential Action -
How action potential is transmitted along myelinated neurone https://youtu.be/mzgTV59su18

A B

Na+

Depolarization
Na+ voltage gated

A channels are open

1. Action potential ( depolarisation ) ..Na+ voltage gated channels open …..sodium influx ..cause
depolarisation at NODES OF RANVIER as the voltage / P.d changing from -70 mv to +40 mv .

2. Action potential stimulate the neigbouring area of the membrane


3. Sodium attracted to area at resting potential ( local circuit ) Na+ ….-ve
4. It will stimulate the opening of the Voltage gated Na+ ions ….( second depolarisation )

Transmission is in one direction due to at A , refractory period and hyperpolarisation ,


recovering from the action potential ( where once we reached +40 mv , sodium voltage gated
channels become inactive , K+ voltage gated channels open , K+ efflux and the membrane
become repolarised ( more negative inside )
5. Myelin sheath is a part which doesn’t get depolarised as myelin sheath prevent movement of ions In or out
of an axon ( electrical insulator preventing leakage of ions )

6. So depolarisation happens only at nodes of Ranvier


7. Local circuit will be set between the depolarised nodes of ranvier and the successive node

8. Action potential jump from one node of Ranvier to the other in a process called SALTATORY
CONDUCTION
Factors affecting the transmission of action potential

1. Myelin sheath

• act as an electrical insulator


• Allow depolarisation only at nodes of Ranvier where there is
no myelin sheath
• Set a localised circuit between adjacent nodes of Ranvier
• So the action potential will jump from one node to another in a
process known as Saltatory conduction
• Allowing faster conduction of action potential ( 0.5 m /sec in
un myelinated vs 100 m/sec in myelinated ) .
• Prevent leakage of ions

2. Diameter of axon

The greater the diameter ( thicker ) of an axon , the faster the speed of transmission ……less leakage ions harder to
maintain resting potential + less resistance+ larger membrane surface are so more ions movement .

3. Temperature

Increase Rate of diffusion of ions ….faster nerve impulse transmission …..till certain temperature ,
above which denature to the protein channels…so impulse fails to be conducted
4. Refractory period

Ensure action potentials separated ….determine frequency of action potentials


Allow action potential to travel in one direction

Synapse A) structure:

Synaptic cleft
Synaptic knob ….contain mitochondria , ER , synaptic
vesicles
Receptor molecules found on surface of post
synaptic membrane

1 . A nerve impulse arrive at the synaptic
cat n knob
o 2. Depolaristaion reach the
3. Calcium ions
diffuse into cytoplasm
of synaptic knob E presynaptic membrane , the
Cavoltage gated Ca+2 channels
E open

4. Calcium ions trigger


the movement of vesicles
5 fuse , release neurotransmitter by exocytosis towards the presynaptic
membrane
I
nnat
i
6. Diffuse across the synaptic
cleft n
7. Acetylcholine bind
to receptors Ligand gated channels
Channel proteins open
…Na+ influx
Synaptic transmission:
Cholinergic synapses( type of synapse which releases acetylcholine as neurotransmitter)
An axon terminal ends in a swelling called synaptic bulb. The membrane here contains voltage gated
calcium channel proteins and the cytoplasm contains vesicles with acetylcholine .

The events that occur when an impulse arrives at a cholinergic synapse are summarised in the diagram

Chemical gated channel


Taster proteins are also known

membrane. as ligand gated channel


proteins .
Neurotransmitters are
cell signaling molecules

r
ab
lG
1. An impulse arrives at the synaptic bulb
iha
2. In response to depolarisation at the presynaptic membrane , the voltage gated channel proteins for
calcium ions open.
R
3. Calcium ions diffuse into the cytoplasm of presynaptic neurone /knob down their electrochemical
gradient . The concentration of calcium ions inside cytoplasm is very low ( almost zero) , so this is a
.N

steep gradient.
4. Calcium ions trigger the movement of vesicles along microtubules towards the presynaptic
membrane .
5. The vesicles fuse with the presynaptic membrane and release their contents of acetylcholine
Dr

molecules by exocytosis .
6. Acetylcholine molecules diffuse across the synaptic cleft and combine with chemical gated channel
proteins on the post synaptic membrane .
7. The channel proteins open to allow diffusion of sodium ions into the cytoplasm of the post synaptic

-cele
neurone down an electrochemical gradient .
8. The post synaptic membrane is depolarised.
9. Acetylcholine molecules leave the protein channels and are broken down by the enzyme
acetylcholinesterase . The products are acetyl groups and choline which diffuse back into the
presynaptic membrane so that choline is recycled into presynaptic neurone.
10. With removal of acetylcholine , this stops continuous depolarisation of postsynaptic
membrane / the postsynaptic membrane is repolarised .
11. If the sum of all the impulses arriving at the post synaptic neurone is greater than its threshold, then
the impulse is sent.
Dr.Nihal Gabr 114
B) function Only study underlined

1. Transport information between neurones …as synapse is found between neurones .


2. Ensure one way transmission …..presynaptic neurone contain vesicles that contain neurotransmitters and
only the post synaptic membrane has the receptors for neurotransmitters …so simply any action potential
would stop at this point .

: Synapses allow integration of impulses


3.
Impulse found at low frequency , do not travel from sensory neurones to reach brain ….filtering out low level
stimuli / low frequency ( infrequent ) impulses …temporal summation.

Allow integration of impulses from different neurones , both excitatory and inhibitory .
Neurotransmitters released by inhibitory neurone , stimulate ion flow that makes them-inside of neurone more
negative ….HYPERPOLARISATION ….this decrease the potential difference makes it more difficult to depolarise
the neurone .

m
4. Interconnection of nerves pathway/. Synapses allow integration of many neurones ..spatial summation .
A) divergence : a single impulse from one neurone can be conveyed to a
number of neurones at a synapse
B) convergence : number of impulses can be compiles into single impulse

5. Synapse are involved in memory and learning


Neurotransmitters Read

Excitatory neurotransmitters Inhibitory neurotransmitters

They open Voltage Gated Na+ channels They open Voltage Gated K+ channels OR Cl-
leading to depolarization of the channels leading to hyperpolarization of the
Postsynaptic membrane/ neurone. Postsynaptic membrane/ neurone.
Example: Acetyl choline Neurotransmitters released by inhibitory neurone , stimulate ion
flow that makes them-inside of neurone more negative
….HYPERPOLARISATION ….this decrease the potential
difference makes it more difficult to depolarise the neurone .
2/8/2023
Part 4
Tongue
Muscles
1. The tongue is covered with many papilla
2. Which has many taste buds
3. Each taste bud has 50 to 100 receptor epithelial cells ( chemoreceptors )
4. Each has microvilli ….that has receptor proteins .

1. Chemicals in food act as a stimulus


2. Bind to receptors proteins which detect salty food
3. Trigger opening of sodium ion channels in cell surface membrane
4. Increase positive charge inside the cell is RECEPTOR POTENTIAL

5. Sufficient stimulation by sodium ions ..the receptor potential will be large


enough to stimulate the opening of the calcium voltage gated channels
6. Calcium diffuse into the cytoplasm ( of receptor cell ) stimulate vesicles to move
and release neurotransmitters by exocytosis from basal membrane .

7. Neurotransmitters stimulate ACTION POTENTIAL in sensory neurone that


transmit impulses to the taste center in cerebral cortex of the brain .

Chemoreceptors act as transducers converting energy of the stimulus into


receptor potential
Read
Muscle structure

1. Sarcolemma : cell surface membrane


2. Sarcoplasm : cytoplasm
3. Sarcoplasmic reticulum : endoplasmic reticulum
4. Many mitochondria in sarcoplasm
5. T tubules …deep infolding into interior of muscle fibres /
extensions from sarcolemma penetrating into cytoplasm .
6. Myofibrils

B) myosin
A) Actin
Thinner, globular protein Fibrous protein

%
Helical structure attached to actin
filaments two important types of
proteins : Thicker long rod
A) tropomyosin …..long thin thread in shaped fibre with
form of fibrous protein wound around
swollen globular
actin filament
heads called myosin
head
B) troponin : globular protein attached
to tropomyosin forming troponin
tropomysoin complex
I band = isotropic band containing thin filaments
A band = anisotropic band containing both thick and thin filaments.

Myofibril

Z line at the middle of every i band


Sarcomere is the adjacent distance between 2 z lines .
How muscle contraction takes place

Muscle stimulation

1. Action potential reach motor end plat


2. Stimulate the calcium Voltage gated channels open ..so
calcium ions diffuse and move into synaptic knob
3. Calcium ions stimulate the vesicles to fuse with
presynaptic membrane and release acetylcholine into
synaptic cleft by exocytosis
4. Acetylcholine diffuse across the synaptic cleft and bind
to receptors on post synaptic membrane ( sarcolemma )
So sodium ions channels open and enter the SARCOPLASM
5. Depolarise the sarcolemma and action potential are
transmitted across the sarcolemma

2. Sliding filament model


6. The action potential travel deep and down the T ubules that
Action potential
Ene branch through sarcoplasm , depolarsation of T tubules .

sta
-

N
W

Sarcoplasm 7. The T tubules are connected to sarcoplasmic


reticulum( already absorbed the calcium from sarcoplasm ) ..the


SR become depolarised , action potential stimulate the calcium
Myofibril channels of SR to open and calcium ions flood out/ diffuse of
SR into sarcoplasm
Sarcoplasmic
reticulum
1. Calcium ions (diffuse out from sarcoplasmic reticulum )bind to troponin
Summary
Troponin changed its shape
Cause the movement of tropomyosin which exposes the binding site of myosin
head on the actin filament ..( ADP is attached to myosin head means head is ata
state to bind to actin filament and form cross bridge )

2.This allows the myosin head attach to the actin filament forming
actin myosin bridge.

3.Once attached to actin filament , myosin head change their angle /


tilt ..pulling the actin filament along towards the center of sarcomere ( power
' and Pi which provide power for
stroke ) ……with the release /detach of ADP
the movement of head . .

4.A new molecule of ATP again attaches to the myosin head , causing
detachemnet of myosin head from the actin filament and change its shape .

5.After this ATPases are activated by the calcium ions released by SR


ATPases catalyse break down of ATP attached to myosin head , this allows
the myosin head to return back to normal position .

6.the myosin head now are detached and can attach to another
binding site on actin filament and repeat the process
7. The process results in the actin filament in one sarcomere being pulled in opposite direction towards each
other
As the filament slide past one another , it causes the sarcomere to shorten ..process called sliding filament
model
Role of the sarcoplasmic reticulum

1. Calcium ions flood out of the SR into muscle cytoplasm ( sarcoplasm ) down a diffusion gradient
2. Some calcium ions attach to troponin
3. Troponin change in shape and move tropomyosin
4. To expose myosin binding site on the actin filament
5. Myosin head now binds / form the cross bridge with actin filament …( ADP attached to the head )
6. Once attached to the actin filament , mysoin head change their angle / tilt ( when ADP leaves
head ) , pulling the actinm filament towards the center of sarcomere….( POWER STROKE ) …
release of ADP powers the movement of the head
7. ATP binds to myosin head , the myosin head then hydrolyse ATP molecules providing energy to
force the head to let go of action / return back to its normal position ( CROSS BRIDGE IS
BROKEN )
8. Now the head returns back to original position , ready to repeat the process

Role of ATP

1. ATP binds again to myosin head , the myosin head then hydrolyse ATP molecules providing energy
to force the head to let go of action / return back to its normal position ( CROSS BRIDGE IS
BROKEN )
2. Now the head returns back to original position , ready to repeat the process
Role of tropomyosin

1. Covers and uncovers myosin binding site on actin


2. When calcium ions attach to troponin
3. Troponin change its shape and move tropomyosin
4. Expose myosin binding site on the actin filament
5. Allowing myosin heads now to bind and form cross bridge with actin thin filaments.

3. Muscle relaxation

1. Calcium ions are actively transported / pumped back into SR using energy from hyrolysis
of ATP
2. This reabsorption of calcium ion allows the tropomyosin to block the actin filament again .
3. Myosin heads are unable to bind actin filaments and coordination stops ( muscle relax) .

rut
Read
How Muscle contract:

r
ab
lG
iha
.N

Myosin head binds to actin when ADP is attached to the


Dr

head .....release of ADP cause the motion /tilting of the


head +actin move-
+power stroke
'r ...cross
ATP binds to head ..hydrolysed ..release energy
bridge broken...head returns back to original position .

The action of the myosin head is similar to the rowing action of rowers in a boat .
The oars ( myosin heads) are dipped into the water , flexed as the rowers pull on
them , removed from the water and then dipped back into the water further along.
The rowers work in unison and the boat and water move relative to one another.
Simultaneously
Dr.Nihal Gabr atsaie 117
Mitochondrion

Sarcolemma

Sarcoplasmic Myosin Actin


T tubule reticulum
Sarcoplasm

B
Coordination in plants
1. Response in venous flytrap

1.
https://youtu.be/O7eQKSf0LmY

Sensory hair cells are deflected when the insect touches them .
My
2. mechanical energy is converted into electrical ….. deflection stimulate the opening
of calcium channel proteins at the base of these hairs .
3. Calcium ions enter cells causing the cell membrane to depolarise
4. At least 2 hairs are touched by insect within 35 seconds ….action potential and
spread over the leaf .
5. When the impulses ( action potential or depolarosisation ) reach the hinge region of
the trap .
Hydrogen ion pump protein in the cell surface membrane respond by pumping hydrogen
ions into cell wall .
Explanation video
6. Decrease in pH in cell wall ..loosening cell wall , breaking the cross links between the
cell wall components ( calcium pectate dissolve in middle lamella ) .
7. So this will cause calcium ions to enter the cell …..decrease water potential
8. So more water will enter by osmosis through aquaporines.
9. Cells expand and become turgid
10. Changing lobes of the leaf from convex to concave closing together and trap the
insect in 0.3S
2. Auxins
Activate
Cell wall
3 expansins
Involved in growth by elongation through acid growth
hypothesis:
2 4 6
1. Auxins bind to the receptors in the cell membrane
2. Auxin stimulate proton pumps in the cell membrane
to actively transport/ pump The hydrogen ions from
the cytoplasm into spaces in the cell wall .
3. Cell wall become acidic ( decrease in pH )
Activate proteins ( expansins ) and to weaken the cell
wall , temporarily break / disrupt hydrogen bonds Cytoplasm
between cellulose microfibrils and dissolve pectin . / Explanation video
break cross links .between cellulose and hemicellulose
Loosening cell wall .
4. Stimulating potassium ions to enter the cells .
5. So decreasing water potential
6. So water will enter by osmosis into cells
Causing an increase in turgor pressure
Cause the cell walls to stretch allowing plant cells to
pH-dependent
grow in size
enzymes activated
3. Gibberellin’s Gene for heigh of plant …..Le ……….dominant allele …..code for functional protein
…that produces an active form of gibberellin GA1.
Water is needed to stimulate the production of
…………………………………..le………..recessive allele gibberellin by the embryo
LeLe ….tall Water needed for hydrolysis


lele…..short ( dwarf) Aleurone layer Where starch is broken into maltose
Water is needed as a medium for reactions

Embryo
Regulate the synthesis Gibberellin
of active form of
gibberellin Endosperm
Amylase
Gibberellin

Starch Maltose
Maltase homozygous recessive lele
Glucose
….apply to it active gibberellin ,
will be stimulated to grow tall

Explanation video
1. Water is absorbed by the seed
Stimulate the production of gibberellin by the embryo within the seed
2. Gibberellin diffuse into aleurone layer .
3. Stimulate the production of amylase enzyme
4. Amylase move into the endosperm cataylse the break down of starch into maltose
5. Then maltlase stimulate the break down of maltose into glucose
6. Glucose transported into the embryo , providing energy as the embryo begins to grow
1. When water enters the seed …stimulate the gibberellin
LeLe by the embryo
2. Gibberellin diffuse to aleurone layer Dominant allele Le codes for functional
enzyme
3.
That produces active gibberellin
1. DELLA protein , inhibit binding of transcription
factor ( PIF) phytochrome interacting protein ….to the
gene promoter ..

2. Gibberellin break down DELLA protein …by binding


to gibberellin receptors ( G1D1) within the cell and which
activates a large complex of enzymes that are able to
break down DELLA proteins.

3. Allowing TF PIF to bind to its target promoter and


transcription of gene. Takes place …resulting in
Genes that promotes growth / cell
production of amylase . ( genes switched on )
division / cell elongation

Role of gibberellin in stem elongation

Acid growth ( involving cell wall loosening )


Where gibberellin Interaction with auxins
Activated Expansins break the cross links in cellulose cell wall
Loosening cell wall
Cell expands when water enter by osmosis
So cell elongation

Increase length of internodes

xyloglucan endotransglucosylase

GA / gibberellin stimulates the cell wall enzyme ( found in stem )


( XET) that breaks the bonds within hemicellulose molecules to loosen
cell wall in a similar way to exapnsins ....so cell can expand when
water enters .

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