Learning and memory Flashcards
What is learning what is memory?
Learning –how experience changes the
brain
Memory –how changes are stored and
subsequently reactivated
What structures in brain are related to learning?
In short-term memory (STM)?
In long-term memory (LTM)?
In short-term memory (STM)?
7 +or - 2 units of information (chunking info allows more)
In long-term memory (LTM)?
No identified limit.
Case study of: Henry Gustav Molaison
What’s his deal?
How do we know?
What kinds of memories tested
– an epileptic who had his medial
temporal lobes removed in 1953 (seizures started in temporal lobes)
- His seizures were dramatically reduced – but
so was his memory
- Mild retrograde amnesia (can’t remember past) and severe anterograde amnesia (cant make new memories)
- time period closet to surgy worst memory is, as it gets further away memory gets better
-1-3 years of retrograde amnesia
- short term memory intact long term severely impaired
How we know this:
Digit span (verbal test) – H.M. can repeat digits as long as
the time between learning and recall is within
the duration of STM
Block-tapping memory-span test (visual/spacial)– this test
demonstrated that H.M.s’ amnesia was global
– not limited to one sensory modality
Other types of memory tested:
Procedural:
Mirror-drawing task – H.M. exhibits
improvement with practice. He is able to show
skill memory – demonstrating that he can
learn some things – although he is not aware
of it.
Rotary purist keep pen on spinning target
H.M. readily “learns” responses through
classical conditioning. (bell-puff of air-blink)
What is amnesia two types?
What kind did hm have?
Retrograde (backward-acting) – unable to
remember the past
Anterograde (forward-acting) – unable to form
new memories
Both: Mild retrograde amnesia (can’t remember past) and severe anterograde amnesia (cant make new memories)
Scientific Contributions of
H.M.’s Case
Medial temporal lobes (hippocampi) are involved in memory
STM and LTM are distinctly separate
ex. H.M. is unable to move memories from STM to LTM, a problem with memory consolidation
Memory may exist but not be recalled
ex. H.M. exhibits a skill he does not know
he has learned (explicit and implicit memory diff)
- Let’s us learn that long term and short term memory are separate
- Hippocampi not involved in short term memories.
- procedural memory is different from other types (not mediated by hippocampi)
- taught us that some regions of brain are more import that others and not all type of memory are from same region.
Explicit Vs Implicit Memories
Explicit memories – conscious memories
Implicit memories – unconscious memories,
Clive wearing
- herpes encephalitis
- severe anterograde and some retrograde
amnesia - similar to hm
- good procedural memory for piano
- few second trail of what your life is
-retained affective memory (emotions)
Repetition priming tests
- used to assess implicit memory
– performance in identifying word fragments is
improved when the words have been
seen before
ex. Hm - If you ask if he’d remember the word, he say no
-if you show him a chunk of the word, he could remember - Implicit memory
Semantic vs episodic
Semantic: facts general info
episodic: episodes of life
- Semantic memory (general
information) may function normally
while episodic memory (events that
one has experienced) does not
– they are able to learn facts, but do not
remember doing so (the episode when
it occurred)
Is short term memory effected by medial tempral legions
No long term memory is
Rb
- R.B. suffered damage to just one part of the hippocampus (CA1 pyramidal cell layer) and developed amnesia
R.B.’s case suggests that hippocampal damage alone can produce amnesia
less severe than hm but still severe
Korsakoff’s Syndrome
- Often a combination of heavy alcohol use with thiamine deficiency
Symptoms:
- amnesia personality changes, intrusions (saying words that aren’t on list), say things that are untrue but not lying (confabulation)
Typically, damage:
in the medial diencephalon
– medial thalamus + medial hypothalamus
Looks like retrograde amnesia gets worse over time, but might not be true. Could just be anterograde amnesia earlier in life.
Unfolds over a long period of time, hard to disentangle in between retrograde amnesia.
Do the Hypothalamic mammillary bodies cause korskoff amnesia?
No its probably just due to damage to the brain as a whole
Alzheimer’s disease
-Often severe atrify of the brain
- Degree of atrify doesn’t correlate highly with neuropsychological functioning
Begins with slight loss of memory and
progresses to dementia
General deficits in predementia AD
Major anterograde and retrograde amnesia in
explicit memory tests
Deficits in STM and some types of implicit
memory – verbal and perceptual
Implicit sensorimotor memory is intact
Pathophysiology of Alzheimer’s
Accumulation of beta amyloid plaques
Typically, glymphatic symptom clears debris in brain
Neurofibrillary tangles strangle neurons to death
Most idiopathic
Genetic form early onset
What damage causes the amnesia seen in AD?
Memory effected first, then medial functioning end stage: global cognition effected
Decreased acetylcholine
Due to basal
forebrain degeneration
- Acetyl Colin in charge of memory and attention
Basal forebrain strokes can cause amnesia
and attentional deficits which may be
mistaken for memory deficits
Medial temporal lobe and prefrontal
cortex also involved
Damage is diffuse – resulting amnesia
is likely a consequence of acetylcholine
depletion and brain damage
Treatment of ad
Acetylcholinesterase inhibitors = more acetylcholine
ChE’s primary role is to rapidly hydrolyze (break down) acetylcholine, preventing its prolonged action and ensuring proper muscle function and nerve conduction.
No direct treatment, just “bandages”
helps it plateau
Traumatic brain injury
- blow to brain
- loss of consciousness
- anterograde amnesia (sometimes retrograde)
- tells us that there is a temporary disruption in consolidation and storage of memory - normal functioning (islands of memories about retrograde amnesia)
Posttraumatic Amnesia
Concussions may cause retrograde
amnesia for the period before the blow and some anterograde amnesia after
The same is seen with comas, with the
severity of the amnesia correlated with the duration of the coma
Period of interograde amnesia
suggests a temporary failure of
memory consolidation
What was heb’s theory? was he right?
Concussions disrupt consolidation
(storage) of recent memories
Hebb – memories are stored in the
short term by neural activity
Interference with this activity
prevents memory consolidation
Blows to the head (i.e., concussion)
ECS (electroconvulsive shock)
Long gradients of retrograde amnesia
are inconsistent with Hebb’s theory
of consolidation
Heb wrong
ECT
Effective treatment for severe depression
But worsens memory
Ex.
Test memories for tv shows that only aired for one season (compare when that tv show aired)
Showed ect only effects memory for tv shows aired 1-3 years ago
Maybe that is the time it takes for memories to be consolidated
What is the typical period of retrograde amnesia?
2–3 years to fully consolidated outside medial temporal lobes
Reconsolidation
When a memory is retrieved from LTM, it is temporarily held in STM
Memory in STM is susceptible to post-
traumatic amnesia until it is reconsolidated
You think about a memory
then you have to reconsolidate it
Here it is susceptible to change
This is how psychotherapy works (constant reframing of memories)
The Hippocampus and
Consolidation
Hippocampus temporarily stores memories
Hm had severe deficits because of damage to
Rhinal cortex: episodic memory
Anterograde amnesia due to damage to the rhinal cortex
- Doesn’t have to be bilateral (left verbal, right visual spacial)
Rhinal cortex legion: issue with consolidating memories
Rhinal cortex involvement lead to amnessia
Lesioning hippocampus and rhinal cortex caused no difference
HM had damage to rhinal cortex. Hippocampus isnt implicated in his type of amnesia
RB only had damage to his hippocampus and had moderate to severe amnesia. Explain how
Ca1 region of hippocampus is heavily connected to rhinal cortex
any region that they are connected to can also be damaged by association
(diaschisis- one region damage causes dysfunction to another region that’s interconnected to it)
Remove hippocampi and rhinal cortex functions more properly
Ischemia-induced hyperactivity of CA1
pyramidal cells damages neurons outside
of the hippocampus.
Extrahippocampal damage is not readily
detectable.
Extrahippocampal damage is largely
responsible for ischemia-induced object
recognition deficits.
Rhinal cortex plays an important role ….
in object recognition
Hippocampus plays a key role in…..
Hippocampectomy produces deficits on……
Many hippocampal cells are place cells– responding when……
- memory for spatial location.
- Morris maze
- a subject is in a particular place
- Morris maze
- study spacial learning or memory
- put mouse in milky water must swim around until they find platform to stand on
Place cells
Cells that fire when in a particular spacial location
Jennifer Aniston
Neurons
Cells that represent a concept
- Friends, her in another move, her name…
All cause the neurons to fire
What memories are stored where:
Hippocampus
Rhinal cortex
Mediodorsal nucleus
Basal forebrain
Hippocampus – spatial location
Rhinal cortex – object recognition
Mediodorsal nucleus – Korsakoff’s
Basal forebrain – Alzheimer’s disease
Damage to a variety of structures
results in memory deficits.
Inferotemporal cortex –
visual perception of objects – changes in activity seen with visual recall
Amygdala
– emotional learning : lesion leads to lack of learned fear
Prefrontal cortex what does it do what if it’s damaged
- Temporal order of events
and working memory - Encoding aspect of memory (left prefrontal cortex)
- Retrieval component of memory reliant on right prefrontal cortex
Prefrontal cortex – damage leads to problems
with tasks involving a series of responses
Cerebellum and striatum
– sensorimotor tasks
Cerebellum – stores memories of sensorimotor skills – conditioned eyeblink,
Striatum – habit formation – associations between stimuli and responses
Long-term potentiation (LTP) –
synapses are
effectively made stronger by repeated
stimulation
Strength of synapse when exposed to repeated stimulation
Ex. a fires b fires 100% of time
By Hebb
LTP
- Found in regions highly involved in learning and memory (ex. medial temporal lobes)
LTP can last for many weeks.
LTP only occurs if presynaptic firing is followed by postsynaptic firing
Co-occurrence is necessary for learning and memory
Neurons that fire together wire together
LTP can be viewed as a three-part process:
Induction (learning)
Maintenance (memory)
Expression (recall)
Induction of LTP:
Learning
Most commonly studied where NMDA
glutamate receptors are prominent
NMDA receptors do not respond maximally
unless glutamate binds and the neuron is
already depolarized
Ca++ channels do not open fully unless both
conditions are met
Ca++ influx only occurs if there is the co-
occurrence that is needed for LTP, leading to
the binding of glutamate at an NMDA receptor
that is already depolarized
Ca++ influx may activate protein kinases that
induces changes causing LTP
Maintenance and Expression
of LTP: Storage and Recall
Pre- and postsynaptic changes
LTP is only seen in synapses where it was
induced
Protein-synthesis underlies long-term changes
Long-lasting changes in extracellular
glutamate levels
