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Learning
Memory
Forgetting
Disorders of memory
Three stages of memory
Encoding/registration
Storage
Retrieval or recall
The major qualitative categories of human memory
(procedural)
Declarative memory
Semantic memory
A piece of data. Theoretical knowledge independent of time
and place.
E.g: A telephone number, knowing that an cat is called to be a
"animal
Episodic memory
Factual knowledge of a specific moment in time and place,
personal experiences
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Procedural memory
Not based on the conscious recall of information, but on implicit learning.
Learning motor skills and should be considered a subset of implicit memory.
Revealed when one does better in a given task due only to repetition (involves
cerebellum and basal ganglia).
Priming: implicit memory in which exposure to a stimulus influences response
to a subsequent stimulus.
Eg: Read a list of words including the word table. If later asked to complete
a word starting with tab, the probability that the answer is table is greater
than if not so primed. Interestingly Alzheimer patients have decreased priming.
Topographic memory
Ability to orient oneself in space, to recognize and follow an itinerary, or to
recognize familiar places.
Getting lost is an example of the failure of topographic memory.
The major temporal categories of human memory
Immediate very large
Working small
Long term - engram
Memory types might communicate
Retention of briefly presented
material depends on context,
experience and meaning
(association)
Priming evidence for transfer
from immediate to long term
Memory is not static, but depends on context
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Motivation can enhance memory
Priming evidence for transfer
from immediate to long term
Repeated exposure does not necessarily lead to memory
Repeated exposure does not necessarily lead to memory
Important to forget unimportant info
(recognize which TV programs had only been broadcast for 1 season)
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What does attention & training do?
increase association
! synaptic plasticity
! changed receptive fields
Hunting in adult increases plasticity (in owls)!
Bergan et al. 2005
Classical conditioning
! Modify innate reflex by associating it with unrelated stimulus
by repeated association.
! e.g. Pavlov: salivation (unconditioned response) to food
(unconditioned stimulus). Pair with bell (conditioned stimulus)
=> salivation upon sound (conditioned response)
Operant conditioning
! Altered probability of a behavioral response by associating
the response with a reward (or punishment).
! e.g. press lever to get food (skinner box)
Conditioning
Receptive field plasticity in A1
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Rapid receptive field plasticity and long term storage
increase in CS sign change in CS!
Rate of consolidation related to pre-training BF distance:
Cells that were tuned closer to the CS, and therefore were more responsive to it,
completed their tuning changes within 1h.
Cells that were tuned to more distant frequencies, and so were less responsive to the
CS, required 3days to complete their tuning shifts.
Attention mediated by cholinergic afferents from
basal forebrain
Can increase excitation
What about attention & training, how does it
work?
Mechanisms of plasticity What circuits are involved in this?
Receptive field plasticity in A1 with pos. reinforcement (by electrical
stimulation of forebrain)
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Long term memory Hippocampus involved in spatial memory
critical in laying down declarative memory,
but is not necessary for working memory,
procedural memory, or memory storage.
Damage to the hippocampus will only
affect the formation of new declarative
memories.
Spatial learning and memory depends on the hippocampus
Memory storage is distributed
Lashley 1920s
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Connections between the hippocampus & possible
declarative memory storage sites
Long term declarative memory is stored in cortex (temporal cortex)
Reactivation of of visual and temporal cortex during
remembering
Visual association cortex is activated when images are recalled
Frontal cortex activated when declarative memory is accessed.
Diseases of memory
Amnesia
Alzheimers disease (we already covered this)
Anterograde amnesia
Drug induced or lesions
Loss of memory of what happens after the event that caused the
amnesia
Patients have widely varying degrees of forgetfulness.
Patients lose declarative memory (recollection of facts) but retain
non-declarative memory (procedural memory).
Can remember & learn how to do things such as talking on the
phone or riding a bicycle, but they may not remember what they
had for lunch.
Patients have diminished ability to remember the temporal
context in which objects were presented.
depicted in movie Memento (2000)
MTL memory system (hippocampus, perirhinal, entorhinal, and
parahippocampal cortex)
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Retrograde amnesia
Unable to recall events that occurred before the development of
amnesia.
New memories can be formed
Lesions or trauma of temporal lobe esp. hippocampus and
temporal cortex
Global amnesia
Some patients have a combined form of anterograde and
retrograde amnesia
time
memory
Areas that, when damaged, can give rise to declarative memory disorders
HM: One of the most famous patients in
Neuroscience
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HM: One of the most famous patients in
Neuroscience
Henry Gustav Molaison (name only revealed after his death 2008)
HM suffered from intractable epilepsy (due to bicycle accident at age 9)
HM suffered from seizures for many years.
HM's epilepsy localized to his L&R medial temporal lobes (MTLs)
MTLs were removed bilaterally as a treatment
HM lost ~2/3 of his hippocampus, parahippocampal gyrus, and
amygdala.
After the surgery, epilepsy was controlled
Died 2008
HM
2/26/1926 12/2/2008
MTL removal
HM
Anatomical Substrate for Declarative Memories
IQ was normal. Perception, abstract thinking and reasoning were
normal
But: There has been one striking and totally unexpected
behavioral result: a grave loss of recent memory in those cases in
which the medial temporal-lobe resection was so extensive as to
involve the major portion of the hippocampal complex
bilaterally!
In [H. M.]!the loss was immediately apparent. After operation this
young man could no longer recognize the hospital staff nor find his
way to the bathroom, and he seemed to recall nothing of the day-
to-day events of his hospital life!he did not remember the death
of a favorite uncle three years previously, yet could recall some
trivial events that had occurred just before his admission!
His early memories were apparently vivid and intact.
HM was very different after surgery
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HM was unable to recall that his family had moved house or that his father had
died.
Some aspects of HMs memory were intact: He could learn motor tasks, but
had to be reminded that he knew how to perform them!
He could remember the floor plan of the house he had lived in for about 8
years, and could draw it accurately.
But when asked to draw the floor plan after moving, he would draw a plan of
his old house.
He never recognized his doctors, despite meeting with them for for over 30
years. He was chained to the past.
HM had an IQ of 118 (above average).
Unlike some patients with frontal lobe damage, HM's social behavior was
normal.
HM's symptoms
HM was very different after surgery
Anterograde amnesia: his working memory and procedural memory
were intact, he could not commit new events to long-term memory.
Retrograde amnesia: could not remember most events 34 days
before surgery, and some events up to 11 years before => amnesia is
temporally graded.
HM's long-term procedural memories were intact: he could learn new
motor skills, despite not being able to remember learning them.
HM was studied for 45 years!
HM did not have long term declarative memory,
but could store procedural memories
HM could learn how to draw a figure
by looking at its reflection in a
mirror
HM could solve the Hanoi towers
problem
What did we learn from HM?
HM had short-term memory and procedural memory but not long term episodic
memory. Thus recall from these memory systems may be mediated by different
areas of the brain.
HM could not create new long-term memories, but could recall long-term memories
that existed before his surgery. Thus encoding and retrieval of long-term memory
information may also be mediated by distinct systems.
After MTL surgery HM did not form new long-term memories of new events or new
semantic knowledge (he lived in the past). Thus the MTL are responsible for the
formation of semantic and episodic long-term memory.
HM performed normally in IQ tests & had normal language abilities. Thus some
memory functions (e.g., short-term stores, stores for words, phonemes etc.) do not
depend on MTL.
HM could remember information over short intervals of time. Thus working memory
does not rely on MTL.
Thus short-term and long-term stores of memory are different.
HM's intact language abilities suggest that language production, comprehension, and
lexical memory, are independent of MTL.
HM could acquire new motor skills demonstrated preserved motor learning. Thus
implicit (non-conscious) memories are not stored in MTL.
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Basal ganglia are involved in non-declarative memory
Probabilistic learning task: Pink door gives reward. But pink door only
appears when right sequence of other doors is chosen
Structures involved in acquisition and storage
Declarative non- declarative
short-term
storage
Long-term
storage
hippocampus &
related structures
unknown...
presumably
widespread
Variety of sites:
Wernickes for
words, temporal
cortex for objects &
faces etc.
cerebellum, basal
ganglia, premotor
cortex, other motor
areas, PFC, etc.
So how does memory get shuttled around?
Brain has oscillatory activity that aid
in this as it synchronizes areas.
~25-70Hz gamma (perception,
consciousness?)
~12-20 Hz beta (active thinking?)
~6 Hz theta (related to arousal?)
Rhythms of the brain: Buszaki
Oscillations synchronize activity between areas
Brain has oscillatory activity that aid
in this as it synchronizes areas.
~25-70Hz gamma (perception,
consciousness?)
~12-20 Hz beta (active thinking?)
~6 Hz theta (related to arousal?)
Rhythms of the brain: Buszaki
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Aging and memory
downhill from here
There is hope: compensatory strategies in aging
High-functioning older individuals use both sides of their PFC
There is hope: compensatory strategies in aging
Larry Katz
1957-2005
There is hope: compensatory strategies in aging
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Standard = impoverished? Enriched = stimulating?
Role of the environment in synaptic plasticity
Environmental enrichment aids in stroke
(ischemia) recovery
+
transplants
-
transplants
normal
impaired
Environmental enrichment helps in Alzheimers
p25 mice => memory impairment
4 weeks of EE => better memory
performance
=> more LTP
=> more synaptic proteins
Enriched environment promotes neuronal branching
Standard environment Enriched environment
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Enhanced cortical thickness
Enhanced brain weight
CREB-mediate gene expression expression
Enhanced dendritic branching
Enhanced oligodendrocyte to neuron ratio
Enhanced number of synapses per neuron
Enhanced ocular dominance plasticity
Decreased inhibition
Enriched environment results in:
Is there an effect of an enriched environment on humans?
London cab drivers have larger brains!
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How to fix memory? How to learn better?
Ampakines:
Long-term potentiation is enhanced & neurotrophic factor (BDNF)
increased in the hippocampus
Methylphenidate (Ritalin):
Indirect catecholamine (dopamine, norepi) agonist
AD/HD drug
Improvements in working memory performance
occur with task-
related reductions in regional cerebral blood flow in the dorsolateral
prefrontal cortex and posterior parietal cortex.
The effects of methylphenidate on working memory were greatest in
the subjects with lower baseline working memory capacity.
Drink coffee!
Caffeine enhances cognitive function and skill performance during
simulated soccer activity., Int J Sport Nutr Exerc Metab. 2009
Exercise !
