Limbic system and learning/memory Flashcards

1
Q

Why did patient HM have memory deficits?

A

He had his hippocampus, perirhinal cortex, and amygdala removed

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2
Q

Declarative memory

A

ability to recollect events or facts that have a specific temporal and spatial context as well as semantic knowledge

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3
Q

Where is declarative memory formed and consolidated?

A

Hippocampus

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4
Q

Where is declarative memory stored?

A

Neocortex. Important in storage of faces

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5
Q

Procedural memory

A

ability to learn new motor skills

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6
Q

What structures process procedural memory?

A

cerebellum, striatum, frontal cortex

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7
Q

What area of brain is activated during face recognition tasks?

A

inferotemporal cortex

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8
Q

Short-term memory

A

memory lasting fractions of a second to seconds. Sensory systems –> sensory cortex

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9
Q

Working memory

A

Memory lasting from seconds to minutes. Dorsolateral prefrontal cortex

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10
Q

Lesion in dorsolateral prefrontal cortex

A

forgetting things like where you left your keys; executive dysfunction; confabulation

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11
Q

Long term memory

A

lasts days to years. Stored in neocortex

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12
Q

Input pathway to hippocampus

A

entorhinal cortex via perforant path –> dentate gyrus –> mossy fibers –> CA3 on Ammon’s horn –> Schaeffer collaterals –> CA1

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13
Q

Output from hippocampus

A

CA3 and CA1 –> fornix

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14
Q

How is LTP induced in hippocampus?

A

repeated stimulation of:

perforant path –> CA3

or

Schaeffer collaterals –> CA1

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15
Q

Molecular basis for LTP

A

simultaneous glutamate excitation and postsynaptic depolarization –> NMDA activation –> Ca influx –> Calmodulin stimulation –> CaM kinase II stimulation –> autophosphorylation of CaM Kinase II –> prolonged activity –> larger EPSP, incorporated and phosphorylated AMPA receptors –> increased glutamate response

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16
Q

associative memory

A

learning to associate several cues with a particular fact or object. Active while playing charades. Induced by LTP

17
Q

learning

A

synapse formation/retraction in somatosensory cortex. neurogenesis in olfactory bulb, hippocampus and cerebellum

18
Q

Alzheimer’s disease amyloid hypothesis

A

A-beta 42 –> synapse loss and neurodegeneration –> cognitive impairment

APP proteolysis by beta and gamma secretases –> A-beta –> neurotoxicity –> failure to maintain LTP in hippocampus

19
Q

Alzheimer’s therapy based on amyloid hypothesis

A

reduce A-beta levels in brain of early AD patients

A-beta antibodies; inhibition of B/y secretase proteases –> blocked APP proteolysis

20
Q

Role of amygdala in emotion

A

4 F’s: Flight, fight, food, sex

removal –> Kuver-Bucy syndrome

21
Q

“Emotional” limbic system

A

Amygdala, Cingulate gyrus, DM of thalamus, ventral basal ganglia (caudate and putamen), insular cortex, hypothalamus

22
Q

Where is emotion expressed and encoded?

A

expressed: hypothalamus and midbrain reticular formation –> autonomic visceral/somatic motor actions

Encoded: limbic system (areas around the 3rd ventricle

23
Q

Conditioned flavor aversion

A

Associative learning

Food + malaise –> avoid that food

24
Q

Does conditioned flavor aversion involve “Pavlovian” conditioning (ie: simultaneous stimulation by different stimuli)?

A

No! You get sick within ~30 min of eating –> robust CFA. Can happen with a single episode of malaise

25
Q

Mechanism of conditioned flavor aversion

A

novel food –> cholinergic neuron activation in basal forebrain –> Ach release to brain –> insular cortex activity –> NMDA receptor phosphorylation (LTP) –> affected NMDA response to input from amygdala

Amygdala receives malaise info from CN X

Stimulation of amygdala + NMDA –> CFA

26
Q

What drug class can prevent conditioned flavor aversion?

A

antimuscarinics. Block cholinergic neuron activation in basal forebrain