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BPK 306 > Molecular Mechanisms Of Learning And Memory > Flashcards

Molecular Mechanisms Of Learning And Memory Flashcards

1
Q

Repetitive activation of an afferent pathway to the hippocampus increases response where?

A

Pyramidal cells

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2
Q

Two phases of LTP

A

Early- insertion of receptors from vesicle stores (min/hrs)
Late- modification of gene expression and structural changes (hrs/days)

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3
Q

What are silent synapses

A

Synapses only have NMDAR. Few or no AMPA can be woken up by LTP

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4
Q

What molecules needed for AMPA insertion

A

High Ca- activates calmodulin and CAMKII
AMPA phosphorylation and exocytosis

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5
Q

Presynaptic LTP pathway

A

Repetitive synaptic activity leads to presynaptic Ca entry - AC - cAMP - PKA - Rab3a and RIM1 (coordinate exocytosis) - exocytosis of glutamate

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6
Q

How are AMPAR removed- LTD

A
  • dynamin/clathrin mediated endocytosis
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7
Q

Name two other LTD mechanisms

A

mGluR
eCB

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8
Q

mGluR pathway

A

Glu binds to mGluR postsynaptic - triggers AMPAR internalization
- process requires rapid protein synthesis (mechanism)
First observed at parallel fibre Purkinje cell synapse

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9
Q

eCB LTD pathway

A

Endocannabinoid
mGluR activation by glutamate - PLC and intracellular Ca initiates synthesis of eCB - eCB travels retrograde to bind to presynaptic cannabinoid 1 receptor (CB1R) - depress NT release
- cannabis facilitates this pathway

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10
Q

Main postsynaptic receptor in cerebellum

A

mGluR

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11
Q

How do cannabinoids work

A

Mostly acyl chain- high hydrophobic - diffuse out of neuron
- travel retrograde

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12
Q

Effect of cannabis on body? location of binding?

A

Bind to CBR - found in hippocampus and substantia nigra (reward, addiction)
- can permanently effect learning and memory

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13
Q

Explain late events of LTP. Why are they important?

A

Important- involve structural changes that maintain plasticity
- AMPA anchored by scaffolding proteins- PSD95,cadherins, catenins
- expression levels of scaffolding proteins change (Cadherins increase)
Cadherins- mediate adhesion through interactions across the synaptic membrane and associate with AMPA
Catenins- couple AMPA to cytoskeleton

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14
Q

How to go from LTP to LTD

A

Late stages of LTP removed first. Early stages removed next
- internalize Cadherins

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15
Q

Memory formation in hippocampus

A

Synapses between excitatory neurons form a new circuit within seconds of event

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16
Q

Long term memory storage location

A

Temporal lobe

17
Q

when do synapses weaken

A

Rlease of NT does not produce an EPSP that reaches threshold
- synapse weakens, circuit may disappear

18
Q

Experimental evidence for LTP link to learning and memory

A
  • in absence of LTP learning and memory is impaired (Giese)
  • LTP is increased during fear conditioning (Rogan)
  • memories can be inactivated and reactivated with LTD and LTP (Nabavi)
19
Q

Place cell experiment

A

Place cells are pyramidal neurons within the hippocampus
Single unit recordings from hippocampus show that specific place cells fire when animal in particular location
- put stimuli (light, food) in specific locations, through simultaneous exposure place cells can fire in response to stimulus even when in different location
- link to learning and memory

20
Q

Mossy fibres

A

High frequency
Constant
Multiple sources
Indirect synapses

21
Q

Climbing fiber

A

Low frequency

22
Q

Inferior olive nucleus

A

Provide input when error (executed doesnt equal intended)
- fires with error

23
Q

Where are climbing fibres, mossy fibres located

A

Cerebellum

24
Q

Function of cerebellum

A

Oversees if movement executed is equal to movement intended
- important in motor learning

25
Q

Role purkinje fibres

A

Sole output of cerebellum. Mossy and climbing send info here

26
Q

Role of climbing and mossy

A

Input to purkinje provide Ca that allows LTD when movement is incorrect (we don’t want to strengthen that pathway)

27
Q

Specific what purkinje cells are and their input

A

Large GABAergic neurons
Receive two types of excitatory input (via synapses)
- one climbing fiber (inferior olive nucleus)
- 150,000 parallel fibres from tiny granule cells of the cerebellum itself (mossy fibers - granule- parallel)

28
Q

When do parallel fibers change strength

A

Only if they are active at same time as climbing fiber

29
Q

How can EPSPs generated by parallel fibers become smaller

A

When both parallel fibers and climbing fiber were coactivated at low frequencies

30
Q

When does the cerebellum have lots of mGluR

A

Function in motor learning. using LTD to reduce strength of synapses to pathways with incorrect execution of intended action

31
Q

When is LTD induced in cerebellum

A

When mossy and climbing fire at same time at low frequency (low Ca release supports LTD)

32
Q

Name diseases with links to LTP/LTD impairment explain main ones

A

Schizophrenia- too much synaptic pruning
Alzheimer’s- loss of plasticity, LTP inhibited, LTD induced, neurodegenerative (remove synapses), cognitive decline
Addiction (drugs of abuse- cocaine)- excessive plasticity (too much LTP), alter synaptic plasticity in brain’s reward circuitry (dopamine) causing wanting of drug more (behaviour changes)
Depression, anxiety, PTSD

33
Q

Drugs of abuse alter synaptic function and plasticity where?

A

Ventral Tegmental Area- part of reward system
- increase dopamine

34
Q

Target of cocaine, amphetamines, ecstasy

A

Target dopamine transport, increasing dopamine

35
Q

How do drugs of abuse increase LTP

A

Increase AMPA/NMDA ratio at glutamatergic synapses

36
Q

Role of morphine with GABA and Glutamate neurons

A

GABA- inhibit GABA release therefore decreasing inhibition caused by GABA indirectly increasing excitation
Glutamate- directly increases excitation

37
Q

Alzheimer’s early and late stages explained

A

Early- amyloid beta (protein- oligomer) is misfolded and activates mGluR
Late- thinning (smaller) and loss of synapses

38
Q

Mice experiment linked to addiction? Explain synapse changes

A

Mice chose cocaine over food
- cocaine changes the AMPAR GluA 1/2 heteromer (which is normal and is not permeable to Ca) to AMPAR Glu 1/1 homomers
(Cocaine changes AMPAR composition)

BPK 306 (18 decks)

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