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neuroscience > Cellular Mechanisms of Learning and Memory > Flashcards

Cellular Mechanisms of Learning and Memory Flashcards

1
Q

What is declarative memory?

A

storage and retrieval that is available to the conciseness and can be expressed ( declared) e.g. phone #s and words of a song, past events.

spatial memory is also declarative

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2
Q

What is non declarative memory?

A

memory that is not available to conciseness : skills, associations, e.g. how to use a phone or how to sing

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3
Q

What type of epilepsy did HM have and what type of was removed to cure this?

A

He had intractable epilepsy i.e. constant grand mal seizures which disrupted his life.

He had bilateral medial temporal lobe resection: his uncut, amygdala, periamygdaloid cortex and 2/3 of his hippocampus were removed

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4
Q

How describe what was intact after H.M’s surgery and what changed

A

His IQ, short term memory, and ( RETROGRADE) memory of events before the operation were normal.

His longer term memory of events post-op (ANTEROGRADE) was not intact. therefore, if he read something and you gave it to him to read again 10 minutes later he wouldn’t know he had already read it.

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5
Q

Did H.M have intact declarative, non declarative, or both forms of memories post-op? ( what did in the star tracing task demonstrate in H.M.?)

A

H.M H.M had non declarative memory post-op and showed normal procedural task ability ( on the third of star tracing test because he had done the task several times.

Although he didn’t remember that he had done the task before he improved because he lacked declarative memory (of past events).

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6
Q

How was R.B ‘s memory impairment compared to H.M’s?

A

R.B suffered anoxia due to cardiac arrest and had more modest impairment. THis pt. had specific bilateral brain damage to the CA1 region of the hippocampus.

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7
Q

What happens to rats w/o hippocampus vs normal rats in the spatial learning and memory pool test?

A

rats w/o hippocampus don’t learn how to get to the platform in the pool in a shorter amount of time.

normal rats use the visual cues like windows, clocks, etc. to navigate their way through the opaque water to the platform in a quicker time after 10 trials because they have declarative memory ( spatial memory).

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8
Q

what areas of the brain are involved in declarative memory?

A

HIPPOCAMPUS, rhinal cortex, amygdala, mammillary body, prefrontal cortex, basal forebrain, fornix, thalamus,

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9
Q

Although the neocortex is not directly an area of declarative memory how is it involved in declarative memory?

A

memories are consolidated and distributed to the neocortex from the hippocampus therefore there are lots of synapses between these 2 regions ( mostly glutamatergic synapses)

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10
Q

what is the difference between immediate working and long term memory?

and how much of immediate working memory become long term?

A

immediate- fractions of seconds
working-seconds to minutes ( e.g searching for a lost object
long-term- days- years

some into from working and immediate make it to long term but most is forgotten

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11
Q

What type of memory is the neocortex very important in?

A

long term

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12
Q

what does long term memory depend on?

A

growth and/or reordering of relevant synaptic connections.

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13
Q

what area of the brain is needed for long term memory of words ( a declarative process)?

A

wernicke’s area

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14
Q

What area of the brain is needed for long term memory of faces and objects ( a declarative process)?

A

temporal cortex

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15
Q

what areas of the brain are involved in non declarative long term memory?

A

cerebellum, basal ganglia, premotor cortex, and other sites related to motor behavior.

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16
Q

What area of the brain are needed for short term declarative memory?

A

hippocampus and related structures

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17
Q

what area of brain is needed for short term non-declarative memory?

A

unknown but presumably widespread

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18
Q

what is intrinsic trisynaptic?

A

3 synapses w/ axons that can be stimulated

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19
Q

intense stimulation of the preforant path leads to what?

A

release of glutamate and LTP ( long term potentiation) in the granule cells.

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20
Q

What happens if there is too much LTP?

A

epilepsy and cytotoxcity

21
Q

What structures are important for declarative memory?

A

hippocampus, medial temporal lobe, midline diencephalic

22
Q

Are all LTP’s the same?

A

no there are diff types, the LTP in CA1 is different than in CA3 for example. ( we focus on CA1 b.c it’s important for declarative memory and the most studied LTP.

23
Q

What is LTP?

A

a Long lasting increase in the synaptic strength that provides and attractive neural mechanism for certain forms of learning and memory

24
Q

Where is LTP commonly observed?

A

at the Shaffer collateral - CA1 synapses in the hippocampus:

pyramidal CA3 neurons in hippocampus send axons to synapse on pyramidal CA1 neurons.

25
Q

What is responsible for the strengthening of synapses that leads to LTP?

A

Calcium ( therefore NMDA receptors are key)

26
Q

Describe the Stimulus 1 and 2 tetanus experiment

A

stimulus 1 is a high intensity/ frequency stimulus for a few miliseconds ( tetanus) to activate postsynaptic CA1 neurons, inducing LTP in CA1 pyramidal cells. ( NMDA at work here in those few seconds)

stimulus 2 is a weak low frequency stimulus that is in a diff set of CA1 synapses. It can’t activate NMDA so MG2+ doesn’t pop off and therefore Ca2+ can’t enter. ( AMPA at work here)

27
Q

What happens if you prevent induction of LTP by giving stimulus 1 pathway an NMDA antagonist at the point where stimulus is usually high frequency and intense?

A

there won’t be any NMDA action so ESPS membrane potential won’t peak or have a higher curve.

28
Q

What happens if you prevent induction of LTP by giving stimulus 1 pathway an NMDA antagonist after the point where stimulus is usually high frequency and intense?

A

the NMDA will still act and a peak and higher ESPS potential will be exhibited because AMPA is working at that point and it won’t be inhibited by an NMDA antagonist.

29
Q

how long does LTP in Shaffer collateral - CA1 synapses in the hippocampus last in vivo?

A

days /weeks as opposed to only hours in vitro

30
Q

What happens to dentritic spine shape when LTP occurs?

A

spine changes shape or appear where they weren’t before when LTP occurs for long term purposes.

31
Q

What is the primary sites of contact btw excitatory synapses and target cells?

A

axodendritic synapes on dendritic spines.

32
Q

What does it mean that LTP is specific?

A

LTP induced by activation of 1 synapse is not observed in another inactive synapse that contacts the same neuron. (it is restricted to only active synapses on a neurons)

33
Q

What does it mean that LTP has associativity?

A

if there is strong stimulation at a synapse the depolarization flows down the to the neighboring synapse and there is weak stimulation of that 2nd synapse accompanying the glutamate release from the first synapse.

34
Q

when do NMDA channels open?

A

only when depolarization is sufficient i.e. high freq. and intensity,

which is needed to remove the Mg2+ and allow Ca2+ to flow into the target neuron.

**glycine is also needed for NMDA activation as it is a co-agonist

35
Q

Is NMDA voltage gated, ligand gated or both?

A

it is a coincidence detector: both ligand gated ( requires glutamate and glycine to bind to it) and voltage gated as it needs a high enough voltage for Mg2+ to be removed.

36
Q

At resting potential is APMA or NMDA active?

A

AMPA only, NMDA needs a higher potential to be activated.

37
Q

What is needed for induction of LTP?

A

NMDA

38
Q

What is needed for maintenance of LTP?

A

AMPA expression in postsynaptic membrane

39
Q

how doe s LTP affect glutamate release and AMPA receptors?

A

LTP increases glutamate release from the presynaptic terminals

LTP enhances the # of AMPA receptors in the postsynaptic membrane.

40
Q

how does glutamate contribute NMDA currents?

A

it promotes Ca2+ release of intracellular Ca2+ stores via IP3 and PKC

41
Q

name 4 kinases that increase intracellular Ca2+ which enhance synaptic transmission and describe how they enhance transmission?

A

PKA (Phosphokinase C)and CAMKII ( calmodulin kinase II ) increase AMPA receptor currents by increasing amount of AMPA receptors in postsynaptic membrane

PKC and PTK increase the NMDA currents.

42
Q

Which 2 kinases enhance glutamate release?

A

PKC and CaMKII

by producing substances that diffuse across the membrane like CO, NO and BDNF

43
Q

What does long term LTP in hippocampus require?

A

gene transcription and protein translation including proteins assoc w. synaptic growth

44
Q

What is LTD?

A

long term depression - a long lasting decrease in synaptic strength that provides an attractive neural mechanism for certain forms of learning and memory

45
Q

Where ia major site of observation aLTD and for how long does it last?

A

the shaffer collateral-CA! synapses when stimulates at low rate ( 1Hz)

for long periods: 10-15 minutes

46
Q

How long does the depression resulting from LTD last?

A

hours

47
Q

How are LTP and LTD similar?

A
  1. they both show input specificity ( activated synapses are needed)
  2. both are NMDA receptor dependent
48
Q

How are LTD and LTP different?

A

LTD has smaller rises in Ca2+ leading to phosphotases dephospho rylation of proteins leading to internalization ( i.e. removal of AMPA receptors from the post synaptic membrane.) thereby reducing synaptic efficacy ( by decreasing sensitivity to glutamate release from schaffer collateral terminals.

LTP has fast rise in Ca2+ leading ti activation of kinases leading to an increase in AMPA receptors on the postsynaptic membrane.

49
Q

WHy is it thought that LTD an LTP have a common synaptic site of action?

A

because LTD can erase LTP and vice versa

neuroscience (32 decks)

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