Learning and memory (plasticity) Flashcards

1
Q

Memory is recall of learned information

A

Process by which information is processed, retained and recovered

Comes after learning

Neural changes/Location associated with storage/recall of information (after learning) is a memory trace/engram

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2
Q

Memory systems are classified by

A

Time - short-term and long-term

Nature – Declarative and Non declarative

Brain systems involved

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3
Q

Where is memory stored?

A

Pathologies, accidents, disorders in remembering, can provide clues about learning and memory

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4
Q

Types of memory

A

Short term: seconds to hours (working memory). Can be erased by shock or trauma

Long term: days to years. Not erased by head trauma

Explicit/Declarative:
Can be reported by an individual, conscious recall, easy to form and forget
Facts, events, people, places (Hippocampus, cerebral cortex)
Episodic: Life events It is very difficult to recreate these memories in other animals
Semantic: Memories of general information

Implicit/Non-declarative:
Cannot be called into conscious recall, tasks learned, tend to require repetition and practice
Perceptual and motor skills (cerebellum, striatum, amygdala)

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5
Q

How is memory formed?

A

Learning – Short term memory – Consolidation – Long term memory

*Not linear. Outcome of several processes.

*Specific memories are not stored in cells (neurons) but rather stored in form of the pattern of signals between cells.

*Starts with the acquisition of new information

*Short term memory (working memory), intermediate memory, consolidation and maintenance of long term memory. This involves transient modifications – ie amount of neurotransmitters released in response to signal, sensitivity of the post synaptic cells to the NTs

*Long term memory can involved permanent structural and functional changes between neurons

*Retrieval causes destabilization and re-stabilization of memories

*Updating and integration with other memories, so memories might change each time they are recalled

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6
Q

Glucosamine and LTP

A

1960’s: synaptic plasticity in glutamatergic pathways

Long term potentiation (LTP)

High frequency stimulation of glutamate neurones → long-lasting increase in efficiency of transmission
(see previous lectures and final slide in notes)

LTD – long term depression can also occur

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7
Q

Long term memory can involve changes in grey matter

A

Functional MRI can measure brain activity

fMRI studies have shown that the hippocampus (right) has a role in spatial memory

Study involving MRI scans of London taxi drivers found

*Posterior right hippocampus was larger in more experienced drivers

*Relative size of the hippocampus correlated with years of experience

London taxi drivers must use their spatial memory to navigate London. Years of such input is reflected in a physical increase in the right hippocampus gray matter volume

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8
Q

Where is memory stored in the brain?

A

Engram: Physical representation or location of a memory

Analysis of memory deficits after brain lesions (animals) or after disorders/accidents (humans)

can give us ideas where different kinds of memories might be stored

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9
Q

Maze learning in rats

A

Karl Lashley studied effect of brain lesions in rat on their ability to learn.

Rats trained through a maze for food reward

Before training: repeated mistakes

After training: went directly to the food

Brain lesions in association areas in the cortex made before training = rats needed more trials to learn to get to the food - lesions interfered with ability to learn

Brain lesions in cortex made after training = rats went down paths in the maze that they had previously learnt to avoid – lesions damaged the memory of how to reach food

Severity of defect correlated with the size, not location of the lesion

Speculated all regions of the cortex contributed to learning and memory

Conclusions incorrect: all regions of the cortex do not contribute equally to memory.

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10
Q

Memory studies in monkeys

A

Macaque monkeys can be trained to visually discriminate shapes

Particular shapes can be associated with food rewards

After training, lesions are made in a visual area in the inferior temporal lobe

The animals can no longer visually distinguish different shapes, ie cannot not remember the visual shape associated with the food reward even though vision is not affected.

Thus, memory for this task specific to vision is stored in a visual area in the cortex

However memory traces are present in multiple regions within the brain

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11
Q

Human case study: Henry Molaison

A

HM suffered from severe epilepsy

Seizure generating medial temporal regions (cortex, underlying amygdala and anterior 2/3rd of hippocampus) removed bilaterally by surgery

Surgery reduced seizures but affected declarative memory:

Long term memory formed before surgery intact (remembered childhood memories)

Short term memory okay (could remember list of numbers)

Procedural memory okay (could learn new skills)

Post-surgery he could not form new declarative memories:

lost the ability to encode new information about his experiences (episodic) or the world (semantic)

-> The hippocampus and median temporal lobes are required for formation and retention of memory

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12
Q

Structures in the median temporal lobes involved in declarative memories

A

Regions of the brain important for explicit memory (declarative memory) are

*the prefrontal cortex (mediates working memory)

*the hippocampus (stores declarative memory)

Ultimate storage site for declarative memory is the cerebral cortex

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13
Q

Object novelty recognition memory

A

Neural pathway of object recognition – a classic test for human memory defecit

Science direct:
“Object novelty recognition is derived from the spontaneous preference demonstrated towards an object which has not been encountered in the past. This preference of a novel object is the result of the retrieval of stored representations from previous experience of other objects.”

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14
Q

Connecting learning regions of the brain

A

Morris Water Maze – the rat tries to navigate unclear water to reach a platform – following cues it can learn the platforms location, one issue is that the rat will likely be highly stressed reducing memory ability and therefore potentially sqewing the data set.

Normal rats quickly learn where the platform is and swim to it

If there is bilateral hippocampal damage the mice cannot figure out how to find the platform

NMDA receptor is key for synaptic modifications in the hippocampus.

If the NMDA receptor is blocked by drugs injected into rats being trained in the water maze, the rats could not find the platform – first evidence that NMDA dependent processes have a role in memory.

( a paper in nature)

HOWEVER: could NMDA have a role in mediating stress instead?

NMDA blockers can reduce psychosis effects for example

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15
Q

3D all in one test

A

Can be used to measure motor, anxiety and memory

Most memories are disposed of aka ‘working memory’ processed in the prefrontal cortex

Cerebellum: memory processing - densest part of the brain (most neurons)

Hippocampus: memory processing – spacial, episodic (life events) etc.

(see diagram in notes for all brain areas involved in memory)

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16
Q

How Alzheimers disease affects the brain

A

Alzheimers results from neuronal loss in memory forming areas of the brain.

The hippocampus (critical for forming new memories) shrinks

The cerebral cortex (responsible for language and information processing) shrivels up damaging areas involved in thinking, planning and remembering

Still a lack of treatment options at present

17
Q

Where does sleep come into learning and memory?

A

More is happening in the brain during sleep than during waking hours!

Processing memories and disposal of misfolded proteins occur during sleep

Histamine is high during waking hours (blue light triggered) and low during sleeping hours

Sleep enhances memories for procedural skills

Stabilises verbal memory etc.
Poor sleep patterns can lead to psychological disorders.

Connected with the consolidation of memory

Interaction between sleep and memory depends on the category of memory

Sleep dependent stabilization of declarative memories (‘what’, recalled consciously) associated with slow wave sleep (SWS)

Sleep can lead to enhancement of all forms of procedural (non declarative) memories (‘how’, cannot be recalled consciously, skills)

18
Q

Stages of sleep

A

The different stages of sleep are defined by: Eye movement, EEG and muscle tone

4-5 cycles of alternating REM and NREM sleep

NREM – 4 stages of increasing deep sleep

19
Q

SWS slow wave sleep

A

*Neuromodulation by NE (Norepinephrine) and 5 HT (serotonin) leads to high reliability of neural network activity in the brain.

*Information appears to flow from the hippocampus to the cerebral cortex where episodic memories are stored

*Flow into the hippocampus (required for formation of new memories) appear to be blocked.

*Physiology of SWS appears to help in reactivating, stabilize, strengthen episodic memories

20
Q

REM rapid eye movement sleep

A

*Neuromodulation by ACh (Acetyl-choline) leads to less reliability of neural activity in the brain.

*Physiology of REM sleep appears to turn off logical reasoning, emotional thinking is up, strong associations are turned down while weak associations are up.

*Helps in identifying weaker associations, modification of concepts, development of insight