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ANAT0012 > Learning and Memory > Flashcards

Learning and Memory Flashcards

1
Q

Two types of LTMs

A

Implicit and explicit

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2
Q

Explicit

A

Conscious, intentional recollection: factual information, past experiences and concepts

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3
Q

Divided into two parts (explicit):

A

Episodic (personal experiences) and semantic (factual information)

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4
Q

What is the hippocampus most important for?

A

Explicit memory, particularly episodic memory (WWW)

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5
Q

External events are represented in the brain by?

A

Spatiotemporal patterns of neural activity - must themselves be the agents of synaptic change

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6
Q

Where must the location of storage, or ‘engram’ of learning and memory be found?

A

Amongst those synapses that support activity-dependent changes in efficacy

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7
Q

Hebb’s postulate

A

Cells that fire together wire together

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8
Q

Gordon Allport’s theory of cell assembly

A

If inputs cause same pattern repeatedly, set of active elements constituting that pattern become increasingly strongly interassociated

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9
Q

What does this activity-dependent, positive-feedback process underlie?

A

Strengthening of effective synapses and facilitates the encoding of LTMs in the hippocampus

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10
Q

Changes in synaptic efficacy first described?

A

Terje Lomo (1966) - persistent increase in synaptic strength - later characterised ‘long-lasting potentiation’ (Bliss and Lomo, 1973)

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11
Q

What does LTP depend on?

A

NMDAR coincidence detector

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12
Q

How is LTP primarily expressed?

A

Increased AMPAR conductance

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13
Q

How can AMPAR conductance be increased?

A

Influx of Ca2+ through NMDAR activates CaMKII which either inserts synaptic AMPARs or phosphorylates existing

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14
Q

Three distinct phases of LTP (ref)

A

LTP1 (2.1hrs), LTP2 (3.5 days) and LTP3 (20.3) - Abraham, 2003

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15
Q

What did Flexner, Flexner and Stellar show in 1963?

A

Intracerebral puromycin led to memory loss of a learning task in mice

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16
Q

In which environment do place cells set up their place fields rapidly?

A

Novel, remain indefinitely stable

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17
Q

What happens if anisomycin is expressed the first time they are exposed to a novel environment? (ref)

A

When returned to the environment, place cell fields showed unstable firing patterns (Agnihotri et al., 2004)

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18
Q

What does PSD-95 do?

A

Stabilises nascent spines, anchors receptors and scaffolding proteins to the membrane

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19
Q

What proteins mediate spine enlargement via actin polymerisation?

A

Actin, CaMKII, Kalirin-7, Rac1

20
Q

Who showed that LTP induction is associated with dendritic spine formation in CA1?

A

Engert and Bonhoeffer, 1999

21
Q

What have several studies demonstrated (DA)?

A

Enhancement of LTP induction and LTM consolidation by dopamine

22
Q

What prevents a weak stimulus from producing LTP when exploring novel environments? (+ refs x 2)

A

D1/5 antagonist ONLY if present during exploration (Li et al., 2003; Frey et al., 1991)

23
Q

Chr2 expressed in what neurons?

A

Dopaminergic VTA in mice

24
Q

Difference in VTA neurons when exploring novel vs familar environments?

A

Significantly more burst firing

25
Q

What was the effect of optogenetic stimulation of VTA neurons?

A

No effect on rate of learning, but following completion of trials there was a clear improvement in the later recall of neural representations of space (McNamara et al., 2014)

26
Q

What do patients with MTL lesions show?

A

Retrograde amnesia that is temporally graded such that recent memory loss is greater than earlier memory loss

27
Q

What is retrograde memory loss restricted to? (ref)

A

Explicit memory, leaving implicit memory intact over time (Scoville and Milner, 1957)

28
Q

What do retrograde memory loss observations suggest? (ref)

A

MTL forms a temporary memory trace needed for explicit memories until they are consolidated to other brain areas, such as neocortex (Squire and Alvarez, 1995)

29
Q

What did Kim & Fanselow (1992) show?

A

Time-limited effect on the fear response of context-conditioned, but not tone-conditioned, animals

30
Q

[K&F] What was the effect of introducing a HPC lesion together with the CFC protocol?

A

Significant reduction in fear response

31
Q

[K&F] What was the effect of introducing a HPC lesion 28 days after the CFC protocol?

A

No difference between controls

32
Q

[K&F] What do they provide evidence for?

A

Storage reorganisation of LTMs to brain regions independent of the hippocampus

33
Q

What is the effect of CA1 fast optogenetic inhibition (even weeks after training)?

A

Blocks remote fear memory recall in CFC mice, which opposes SC model

34
Q

What happened when CA1 inhibition was extended to match the time course of pharmacological blockade?

A

Remote hippocampal dependence converted to hippocampal independence

35
Q

What did the inactivation of ACC lead to?

A

Prevented the recall of behaviours learned a month or more in the past

36
Q

What do Goshen’s et al. (2011) observations suggest?

A

Memories consolidate to cerebral cortex, and while their retrieval is normally dependent on the hippocampus, it can adaptively shift to other brain regions

37
Q

What did Lui et al., (2012) identify, and how?

A

Small subset of DG neurons by exposing mice to a shock in context B which induced expression of ChR2/cFos

38
Q

What did optogenetic stimulation of DG neurons do in a neutral context?

A

Still drove freezing

39
Q

How did Ryan et al., (2015) extend this concept?

A

Also labelled input axons from EC

40
Q

What did Ryan et al. find?

A

Engram cells (DG neurons) had stronger connections from EC afferents, as well as higher spine densities, only if consolidated

41
Q

[Ryan] What did optogenetic stimulation of engram cells lead to?

A

Drove freezing even in the absence of consolidation - memory trace is always present but consolidation may link this to other neurons in the network

42
Q

What is memory reconsolidation?

A

Process of previously consolidated memories being recalled and actively consolidated

43
Q

What does the retrieval of LTMs cause?

A

Once consolidated, LTMs thought to be stable, but their retrieval of a memory trace can cause a labile phase that requires an active process to make the memory stable after retrieval is complete

44
Q

Who first showed the lability of memory?

A

Misanin et al. 1968 - ECT after brief presentation of conditioned stimulus led to memory loss

45
Q

What early studies treating OCD, delusions and depression were noteably successful? (ref)

A

Patients not anaesthetised and asked to focus on compulsions (Rubin, Fried & Franks, 1969)

46
Q

What is the effect of blocking protein synthesis in higher brain regions (e.g. amygdala)? (ref)

A

Prevents reconsolidation of memories, almost completely abolishing the fear response (Nader, Schafe & LeDoux, 2000)

47
Q

Labile phase of memory is a great candidate for targeted clinical interactions, for example:

A

Kroes et al., 2014: ECT in patients with unipolar depression disrupted reactivated, but not non-reactivated memories, for an emotional episode in a time-dependent manner

ANAT0012 (3 decks)

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