learning + memory Flashcards

1
Q

retrograde vs anterograde amnesia

A

anterograde = unable to form new memories

retrograde = unable to recall past memories (memory loss)

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2
Q

role of hippocampus in learning/memory

A
  • hippocampus is highly conserved neural structure across mammalian species.
  • most investigated brain region for memory processes.
  • important for declarative and spatial memory
  • as in HM, patients with bilateral damage/lesion to hippocampus have profound anterograde amnesia
  • in rodents, hippocampus important for spatial learning
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3
Q

role of the striatum in learning/memory

A

• cognitive functions such as
– motivation
– learning habits/addiction

  • dysfunction of striatum underlies neurological (such as parkinson’s disease) and psychiatric conditions (such as obsessive compulsive disorder)
  • unsure exactly how it functions
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4
Q

role of the amygdala in learning/memory

A
  • key centre for associative learning and memory
  • aberrant activity in the amygdala is thought to underpin anxiety and panic disorders
  • in humans, bilateral damage or loss of amygdala profound loss recognising stressful/fearful facial expressions
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5
Q

role of the cerebral cortex in learning/memory

A
  • likely to be location of long term memory (HM’s childhood memories were intact)
  • also priming type of learning such as auditory and visual priming (HM performed well in priming experiments)
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6
Q

role of the cerebellum in learning/memory

A
  • key role in non-declarative learning and memory (dancing, swimming, driving)
  • probably plays a role in other types of memory as well.
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7
Q

describe the T-maze test

what is the affect of silencing the hippocampus / striatum during this test

A

rat placed in T-intersection with a reward on the right pathway

after 1 week training, rat turns to right on the test i.e. places cue

after 2 weeks, the maze is flipped 180º. rat turns to left on test i.e. habitual response

silencing the hippocampus impairs ‘place’ recognition but no effect on habit response

silencing striatum affects habit response but no effect on ’place’ recognition

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8
Q

how does LTP induce both biochemical and biophysical changes?

A

LTP = long term potenation
repeated firing of one neuron to another strengthens the connection and increases the efficiency of the firing

pre-synaptic neurons (especially excitatory) make synaptic contacts on the dendritic spines of post-synaptic neurons = BIOCHEMICAL

LTP leads to increased insertion of additional receptors in the dendritic spine of the post-synaptic neuron

LTP induces formation of of new dendritic spines = BIOPHYSICAL

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9
Q

associative property of LTP

A

LTP can be induced on a weak pathway by pairing with a strong pathway

associative property of LTP is considered as correlate for associative learning process

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10
Q

compare LTP and sensitisation

A

SENSITISATION:
• occurs in spinal cord in vertebrates + invertebrates
• sensitisation of one pathway enhances overall excitability to other stimuli
• example: pain pathways

LTP:
• occurs in brain of vertebrae
• pathway specific
• associative property: weak pathway can be potentiated when combined with strong pathway during potentiation

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11
Q

what determines LTP or LTD?

A

time of spike determines type of plasticity

LTP = presynaptic inputs before/synchronous with postsynaptic spikes (evoked by a second pathway or by current injection)

LTD = presynaptic input followed postsynaptic spikes

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12
Q

what are the short and long term effects of plasticity?

A

SHORT-TERM:
• ↑ in pre+post synaptic [Ca2+]
• ↑ post synaptic receptors

LONG-TERM:
• gene expression
• protein expression
• structural changes

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13
Q

how does epilepsy occur?

what is the kindling model of epilepsy?

what are the similarities between LTP and kindling?

A

long-term LTP induces epilepsy
• distorts conscious perception
• seizures
key feature is aberrant high freq. electrical activity in ECG

kindling model:
• a seizure may increase the likelihood that more seizures will occur
• repeated stimulation lowers the threshold for more seizures to occur
• key regions involved include the amygdala and the hippocampus

both kindling and LTP:
• require high frequency stimulation 
• cause synaptic facilitation
• require protein synthesis
• cause structural synaptic changes
it is thought that changes that occur during LTP during memory formation when goes unchecked may lead to aberrant excitability (as in kindling) and epileptogenesis
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14
Q

what is a cell assembly?

A

neurons are organised into networks with frequent connections

if one neuron is activated, activity spreads extremely rapidly throughout the networks

this network of circuits = CELL ASSEMBLY

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15
Q

how do oscillations in brain activity correlate to behaviour?

A
most frequent oscillations
1. alpha
2. beta
3. theta
4, gamma
least frequent oscillations

different behaviours generate different types of oscillations

there are correlations between how networks are activated and the types of behaviour exhibited by an organism

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16
Q

describe the cellular and network activity of the hippocampus in spatial learning

A

CELL ACTIVITY
• during navigations, cells spike in specific locations to mediate learning
• these cell spikes are relayed during sleep for memory consolidation

NETWORK ACTIVITY:
• during navigation, gamma oscillation occurs in the hippocampus cell assemblies
• this mediates active spatial learning
• this learning is consolidated during sleep:
– same neurons fire again during sleep
– neurons fire in clusters and ripples
– occurs in slow-wave oscillation

17
Q

what is the phase sequence?

A

cell assemblies chain together via an internal mechanism

facilitates rapid memory recall