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HMB200 > Lecture 7 - Learning & Memory > Flashcards

Lecture 7 - Learning & Memory Flashcards

1
Q

________ is a relatively permanent change in behaviour resulting from experience

A

Learning

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2
Q

What is it called when the brain changes with experience?

A

Neuroplasticity

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3
Q

Neuroplasticity is ubiquitous, what are some examples?

A
  • learning information
  • learning motor skills
  • stroke rehabilitation
  • postnatal neurogenesis
  • meditation
  • adjusting to trauma
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4
Q

What changes may be the basis for memory and behaviour?

A

The areas that are ‘engaged’ by an experience may change over time

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5
Q

Synapses are modifiable. Changes in the _____________ might be important for many behaviours

A

Strength of synapses

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6
Q

Hebb’s Postulate

A

When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased

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7
Q

What compelling evidence obtained by Bliss + Lomo was found within the hippocampus?

A

high-frequency stimulation of synaptic connections lead to a persistent increase in their strength

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8
Q

What was the phenomenon founded by Bliss + Lomo called?

A

Long-term potentiation (LTP)

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9
Q

What is LTP?

A

The same stimulation from neuron A generates a bigger response (EPSP) on neuron B

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10
Q

4 steps in experimentally measuring LTP

A
  1. EPSP before stimulation
  2. Tetanic stimulation
  3. Brief, large EPSP increase immediately after stimulation
  4. Lasting, smaller but significant EPSP increase long after stimulation
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11
Q

___________ represent the collective response of a large population of neurons (i.e. many EPSPs)

A

Field excitatory post-synaptic potentials (EPSPs)

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12
Q

Features of LTP

A
  • experimentally induced by high-frequency stimulation (conditions similar to those created by learning stimuli)
  • long-lasting (hours to weeks), which makes it a suitable candidate for long-term memories
  • correlated with memory in many animal models (when strong, learning/memory tended to be strong and vice versa)
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13
Q

One well studied form of LTP covered in class

A

n-methyl-D-aspartate (NMDA) receptor dependant LTP - mediated by post-synaptic changes

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14
Q

Where is NMDA receptor dependant LTP observed?

A

The hippocampus - brain area involved in learning and memory

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15
Q

AMPA/Kainate receptors

A

If bound by glutamate ions can flow in/out

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16
Q

NMDA receptors

A

Have Mg+ block, cell must be depolarized to remove block and to let glutamate bind so that ions can flow in

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17
Q

Steps in NMDA dependant LTP

A
  1. Activation of AMPA receptor by glutamate
  2. Cation influx (Na+)
  3. Depolarization
  4. Mg2+ blockade relieved
  5. Cation (Ca2+) influx
  6. Intracellular cascades
  7. Increased AMPA receptor expression
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18
Q

Manipulations of NMDA receptors that may effect NMDA-receptor dependant LTP, learning + memory

A
  • blocking NMDA receptors blocks LTP + impairs learning/memory
  • genetic knockout of NMDA receptors blocks LTP + impairs learning/memory (subtle effect)
  • genes for NMDA receptors are associated w/ intelligence in humans
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19
Q

_____________ variations in synaptic strength such as LTP may be a fundamental mechanism by which we acquire and modify all behaviours

A

Activity-dependant

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20
Q

The opposed process of LTP, __________, is also linked to memory

A

Long-term depression

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21
Q

LTD in the cerebellum has been proposed as a mechanism to explain ________

A

Motor learning

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22
Q

What is the importance of LTD?

A
  • supporting motor learning
  • resetting of synapses (may prevent saturation of excitation and allow for more flexibility in how neurons change over time)
  • eliminate less useful synapses, allowing for streamlining of existing networks
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23
Q

There are other forms of plasticity, some of which occur at the __________ instead (e.g. enhanced neurotransmitter release from neuron A)

A

presynaptic terminal

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24
Q

What is a drawback of plasticity studies?

A

Most are performed in animals, so most approaches are correlative

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25
Q

Certain neurons change their firing rate with experience

A

Rate remapping (e.g. neuron A fires at a higher rate)

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26
Q

The neurons that fire will change with experience

A

Population remapping (e.g. neuron C did not fire originally, now it does)

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27
Q

Neuroplasticity involves a change in a group of neurons. If the group of neurons is large enough, we might see a visible change in overall _________ when doing an imaging scan

A

gray matter

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28
Q

What did they find in London taxi drivers?

A

Increased posterior hippocampus gray matter in taxi cab drivers

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29
Q

What is memory?

A

A process whereby information is stored, consolidated + retrieved

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30
Q

Different types of memory

A

Sensory, short-term, long-term

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31
Q

True or False: our memories are accurate

A

False

32
Q

Memory over time

A
  • memories for everyday + emotionally arousing events become inaccurate over time
  • confidence in arousing memories remain high
33
Q

Inconsistent information can alter our memories, while other interventions can create memories that never happened, what is this known as?

A

False memories

34
Q

A subset of cells representing a memory is termed a __________

A

Memory trace/engram - thought to include cells that were active during the original experience

35
Q

The cells in the engram are __________; if you activate one cell you might activate __________

A

interconnected, them all

36
Q

What cells are most likely to be included in an engram?

A

The cells that are most excitable/plastic at the time of the experience (the fitness of cells change over time)

37
Q

Events that change behaviour (i.e. induce learning) do so by altering _________

A

gene expression

38
Q

How is gene expression regulated?

A

By transcription factors, which are activated by events associated w/ learning

39
Q

One transcription factor of interest is ________

A

CREB (cyclic AMP-response element binding protein)

40
Q

Learning-evoked changes in genes

A
  • cellular events associated w/ learning activate CREB
  • CREB then activates other genes, altering overall protein expression
  • neurons overexpressing CREB are more likely to be incorporated into an engram
41
Q

Experimental support of regulation by CREB

A
  • neurons overexpressing CREB are more active during fear memory training
  • killing CREB-overexpressing neurons after the fear training impairs the fear memory
42
Q

Who studied where memory was located in the brain?

A

Lashley measured memory in animals w/ cortical lesions:
- memory impairment was correlated with extent of coritcal damage
- no specific cortical region was more important than the other
- suggested that all of the cortex was important (i.e. no localized engrams exist)

43
Q

What did Lashley’s experiments not address?

A
  • subcortical areas (including the striatum)
  • did not consider multiple types of memory
44
Q

One key brain area involved in memory is the _______

A

Hippocampus

45
Q

What did patient HM demonstrate?

A
  • had anterograde amnesia (inability to form new memories) after the hippocampus and adjoining areas were removed to treat his epilepsy
46
Q

Standard memory consolidation

A

New memories are required for hippocampal networking

47
Q

Problems with standard memory consolidation

A
  • other patients with hippocampal damage showed retrograde amnesia
48
Q

Multiple trace theory

A
  • each time a rich, detailed memory is recalled, the hippocampus lays down a new trace of it
49
Q

Summary of the HPC involvement in memory

A
  • the HPC is critical for memory acquisition, but is likely a gateway site rather than a storage site
  • according to consolidation theory, the HPC is involved in recent but not remote memories
  • according to multiple-trace theory, the HPC is important every time a remote episodic memory is reactivated if that memory is rich in detail
  • hippocampal involvement changes over time
50
Q

Forms of memory that the HPC is not required for

A

nondeclarative: skill learning, priming, conditioning

51
Q

Priming

A
  • subconscious preparation improves the performance of a task
  • e.g. previous exposure to object features improves object identification without awareness
52
Q

Recognition memory processes

A

Linked to the perirhinal cortex:
- in animal, perirhinal cortex lesions impair recognition

53
Q

The perirhinal cortex is linked to _______ memory while the hippocampus is linked to ________ memory

A

recognition (visual), spatial

54
Q

Improving memory acquisition

A
  • activation of certain brain areas (e.g. entorhinal cortex) using electrodes can facilitate spatial memory
55
Q

___________ is the use of direct electrical stimulation (via implanted devices) to affect behaviour and perhaps enhance memory

A

Neuroprosthesis

56
Q

What non-invasive tool can you use to measure brain stimulation and improve memory recall

A

TMS

57
Q

Erasing a fear memory engram

A

Ablation of allocated neurons seen in a fear engram in mice

58
Q

Creating false memories

A
  • use transgenic mouse model where active (i.e. engram) cells will express light-sensitive receptors
  • animal is placed in context A (safe): after engram A cells express light-sensitive receptors
  • animal is then placed in fear context B (unsafe): during this time, engram A cells activated with light
  • animal is returned to context A
  • this creates an aversive experience in A that never happened before
  • turned ‘safe memory’ into a ‘fear memory’ by manipulating the engram cells
59
Q

Modifying memories

A

Aversive memories can be highly disruptive to our lives (as in post-traumatic stress disorder/PTSD):
- the amygdala adds ‘emotional valence’ to memories
- this effect is eliminated when the amygdala is damaged or B-adrenergic receptors are pharmacologically blocked (drug intervention)
- a B-adrenergic receptor blocker applied during reactivation reduces PTSD symptoms

60
Q

Symptoms of Korsakoff Syndrome

A
  • Anterograde amnesia
  • Retrograde amnesia
  • Short-term memory loss
  • Confabulation
  • Lack of insight
  • Apathy
61
Q

Causes of Korsakoff syndrome

A

Proper nutrition is vital to the maintenance of the brain:
- caused by a deficiency in vitamin B1 (thiamine) and is often associated with prolonged alcoholism
- thiamine deficiency has major consequences for the health of neurons because thiamine is a co-factor for enzymes involved in carbohydrate metabolism

62
Q

Thiamine as an enzyme co-factor

A
  • Thiamine is an important co-factor for many enzymes involved in carbohydrate metabolism
  • Deficiency of thiamine impairs these enzymes
  • With impaired enzyme function, we might see mitochondrial damage, oxidative stress, and apoptosis
63
Q

The brain in Korsakoff syndrome

A

Reduced volume of the:
- hippocampus
- mamillary bodies
- dorsomedial thalamus

  • Increased volume of the ventricles
  • Damage to the cerebellum is also evident
64
Q

Why does the DM thalamus matter?

A

Through its connections with the PFC and other structures, the DM thalamus is believed to play an important role in memory and other forms of cognition

65
Q

Symptoms of Alzheimer’s disease

A
  • loss of memory
  • language problems
  • difficulty in doing simple tasks
  • disorientation in time and space
  • loss of reasoning capacity
  • difficulty in having elaborate thoughts
  • loss of objects
  • mood changes
  • behavioural changes
  • loss of initiative
66
Q

Alzheimer’s disease

A
  • Progressive, incurable disorder
  • No real treatments
  • Most common form of dementia, affects ~40 million peoples (# expected to double by 2040, 10-15% of people over age 65)
  • Care is very costly due to high level of impairment (~$214 billion in 2014)
67
Q

Genetic risk factors for AD

A

May account for ~20% of cases.

Though many genes are likely involved, three genes in particular have been implicated:
- APP (amyloid precursor protein) gene
- Presenilin genes (which help convert amyloid precursor protein in amyloid-beta)
- ApoE4 (apolipoprotein E4) gene, which inreases cardiovascular risk

68
Q

AD diagnosis

A

Combined approach:
- Patient history
- Collateral history from relatives
- Clinical observations

To exclude other pathology, medical imaging is used:
- detects overall neuronal loss characteristic of AD
- diagnosis can be confirmed with high accuracy post-mortem

69
Q

Diagnostic tools in AD

A

Neuropsychological tests such as the mini-mental state examination (MMSE) to assess cognitive impairments:
- more comprehensive tests needed, especially in early stages

Psychological tests for depression are also used:
- depression can either be concurrent with AD or an early sign of cognitive impairment

70
Q

Features of AD

A
  • progressive neuronal loss
  • beta-amyloid plaques
  • neurofibrillary tangles (involving tau)
  • reduced acetylcholine transmission
71
Q

Plaques in AD

A
  • Extracellular plaques (aggregates of beta-amyloid protein) may be neurotoxic and may interfere with neuronal communication
  • Plaques may arise due to impairments in the regulation (i.e. metabolism and clearance) of APP
72
Q

Acetylcholine System in Aging/AD

A

Acetylcholine is a neurotransmitter importantly involved in memory and cognition. The Basal Nucleus of Meynert is a critical site for acetylcholine projections. This nucleus is affected in aging + AD

73
Q

Cholinergic Hypothesis of Aging/AD

A

Deficiency of acetylcholine is a key factor in cognitive decline associated with aging and AD

74
Q

Treatment of AD

A

Inhibiting acetylcholine metabolism to boost acetylcholine activity

75
Q

Noradrenergic Transmission in AD

A
  • The locus coeruleus (LC) is the principle site of noradrenaline synthesis in the brain
  • LC pathology is also often found in AD and in natural aging
76
Q

Biomarkers for AD

A
  • Allows for early detection and preventative measures
  • Recent focus on biomarkers in the blood, great potential

HMB200 (6 decks)

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