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PN3313 > Learning and Memory > Flashcards

Learning and Memory Flashcards

1
Q

What is a neuronal explanation of learning?

A

Process causing lasting changes in synapses and/ore neuronal activity

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2
Q

What is a neuronal explanation of memory?

A

Changes in synaptic/neuronal activity that persist

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3
Q

How can memory be classified in terms of time course?

A

Short term memory (working memory)

Long term memory

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4
Q

What categories can long term memory be further divided into?

A

Declarative - episodic + semantic

Non-declarative - implicit

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5
Q

What is episodic memory and what brain areas is it associated with?

A

memory for events

temporal lobe and hippocampus

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6
Q

What is semantic memory and what brain areas is it associated with?

A

Memory of different facts

Involves many brain areas with some being category specific

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7
Q

What brain areas are associated with implicit memory?

A

Amygdala, striatum, neocortex, cerebellum and spinal cord

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8
Q

What is priming and what are the two types?

A

Where exposure to one stimulus influences a later stimulus response can be:
conceptual or perceptual

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9
Q

What is procedural memory and what are the two stages?

A

Proceeds with repetition
Cognitive: pay attention to performance (parietal and inferior temporal cortex)
Autonomous: skills executed without much conscious effort (inferior temporal)

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10
Q

What are the two types of conditioning?

A

Classical (two stimuli) and operant (action and consequence)

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11
Q

What is nonassociative learning?

A

About a single stimulus can be:
Habituation - response weakens following bening stimuli
Sensitization - response strengthens following noxious stimuli

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12
Q

How does habituation occur is aplysia?

A

Short term: fewer vesicles available for release from sensory neuron to motor neuron (depression of glutaminergic release)
Long term: decreased number of synaptic contacts

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13
Q

How does sensitization occur in aplysia?

A

Tail shock activates tail sensory neuron which activates a modulatory interneuron which releases serotonin on to the presynaptic area of where the siphon sensory neuron connects to the motor and interneuron. This enhances vesicle release and increases excitation.

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14
Q

What is the biochemical explanation for increased glutaminergic release in aplysia during short term sensitisation?

A
  • Seretonin released my facilatory interneuron binds to either G coupled receptor or PLC coupled receptor
  • Activated G protein dissociates from receptor and activates adenylyl cyclase going on to activate cAMP
  • cAMP binds to PKA, releasing catalytic subunits capable of phosphorylating K channels
  • When depolarisation occurs, fewer open K channels means that Ca2+ enters cell for longer allowing more vesicles to be released
  • PLC activates second messenger DAG which facilitates movement of vesicles
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15
Q

What is the biochemical explanation for increased glutaminergic release in aplysia during long term sensitisation?

A
  • Increased training leads to cAMP (activated by G coupled protein) to release catalytic unit and bind to CREB (cAMP response element binding-protein) which bond to CRE (cAMP response elements)
  • This increases transcription of downstream genes causing increases in proteins such as ubiquitin hydroxylase which causes a degredation of the regulatory subunit of PKA, causing some catalytic units to be persistently active no longer requiring seretonin
  • Also increases transciption of C/EPB which is another transcription factor which aids in the transciption of other unknown genes believed to increase number of synaptic contacts
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16
Q

How does classical conditioning occur within aplysia?

A

Same as sensitisation with addition of:

  • Ca2+ influx binds with calmodulin
  • Binds to adenyl cyclase (coupled with G protein receptor - remeber sensitisation) enhancing reception of serotonin
  • Leads to more cAMP and more facilitation
17
Q

What are the cortex related mechanisms of fear conditioning?

A
  • Increased activity in the lateral nucleus of the amygdala
  • In mouse whose feet are shocked when tone is heard, stimuli from ears and feet either take a direct or indirect pathway from the thalamus and glutaminergic inputs converge on the lateral amygdala causing facilitation
18
Q

What are the short term mechanisms of fear conditioning at a neuronal level?

A
  • NMDAR and voltage gated calcium channel activation
  • Ca2+ influx
  • Inseration of AMPARs (enhanced transmitter release)
19
Q

What are the long term mechanisms of fear conditioning?

A
  • cAMP-dependent PKA and MAPK

- Activation of CREB and gene expression increasing synaptic connections

20
Q

What are the mechanisms of procedural learning?

A
  • LTP forms at synapse from cortex to striatum
  • LTP mediated by NMDARs
  • Maintenance of LTP involves CREB function
21
Q

What brain areas are associated with explicit learning?

A

STM - prefrontal cortex (short term)
LTM - hippocampus (hours-lifetime)
Cortex - permanent storage? (permanent storage)

22
Q

How is working memory belived to be maintained?

A

Through peristent firing maintained by intrinsic properties

  • Depolarisation of pyramidal entorhinal neuron causes opening of v-gated Ca2+ channels
  • These activate Ca2+-active non selective cation channels (CAN)
  • Causes further depolarisation (after depolarisation - ADP) with positive feedback loop that can persist for several minutes
23
Q

Name 3 other mechanisms that can cause persistent firing?

A

Long range - between different brain regions such as the inferior temporal, prefrontal and parietal
Local feedback between neuron groups in a certain area
Mutual inhibition networks (half centre hypothesis)

24
Q

What are the two mechanisms whereby long-term explicit learning is carried out

A

Direct and Trisynaptic take input from entorhinal cortex

3 regions with 4 glutaminergic synapses all capable of forming LTP

25
Q

What is the direct prefrontal pathway?

A
  • Non-associative LTP, requires strong activation on presynapse
  • Dependent on NMDA and v-dependent receptors
26
Q

What is the schaffer collateral pathway?

A

Associative LTP formation where NMDARs are essential
1. Have V-dependent Mg2+ block which is removed by post synaptic APs
2. Binding of glutamate predicts presynaptic activity
Increased Ca2+ activity triggers cellular cascade leading to LTP induction
Hebbs Law - Neurons that fire together wire together

27
Q

How is the CA1 pertinent to spatial memory?

A
  • NMDAR NRI mutation in this region results in failure to induce LTP in mice and poor performance in a water maze
  • NMDAR NR2B overexpression causes smart mice
28
Q

How does long term depression rely on NMDARs?

A

Low levels Ca2+ activate phosphatase calcineurin leading to the endocytosis of AMPARs and therefore LTD

29
Q

What is the hypothesized role of LTD in spatial memory?

A

Needed for preventing LTP saturation
Mutant mouse with phosphatase 2A inhibited causes failure to form LTD in CA1 region also take longer to adjust to a change in location in the water maze

30
Q

What are place cells?

A
  • Found in CA3 and CA1 region
  • Only fire when animal is in certain location in certain environment
  • Formed within minutes and are stable for weeks/months
31
Q

What are grid cells?

A

Found in the medial entohrinal cortex and fire only when animals are in regular triangular knots in the environment
different grid cells have different knot positions/distances
Independent of visual cues, speed and direction (measure distance)

32
Q

Describe LTP formation at the Mossy Fibre pathway (granule and pyramidal cells)

A
  • non-associative (no post-synaptic activity)
  • tetanic stimulation leads to a greater Ca2+ influx and an activation of Ca2+-Calmodulin dependent adenlyl cyclase
  • cAMP increase leads to PKA activation which phosophorylates RIM1a on vesicles
  • Results in enhanced vesicle release
  • Subcellular changes depend on PKA activity
33
Q

What is the early phase and the late phase of the Schaffer pathway?

A

Early - insertion of AMPARs on post synaptic membrane and enhancement of transmitter release
Late - New synapses

PN3313 (9 decks)

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