Lecture 21- Molecular mechanisms of memory Flashcards

1
Q

Where is the hippocampus?

A

-primitive part of cerebral cortex located medially in temporal lobe

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2
Q

When is the hippocampus active?

A

during consolidation phase of explicit memory

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3
Q

What does the failure of consolidation result in?

A

-no formation of long term memory -appears in alzheimer’s

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4
Q

What happens when the hippocampus is damaged?

A
  • prevents formation of new long term explicit memories but does not disturb already formed memories -Does not prevent formation of implicit memories (but can’t remember how you formed them)
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5
Q

What role does hippocampus play in explicit memory?

A

-central to explicit memory= cannot form it without it -the transmission from working memory to explicit long term memory -becomes active again during the consolidation process (when you’re asleep) -part of tuning of memories, need to be able to weight the balance of memories, what happened today, yesterday etc.

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6
Q

What does it mean that memory is associative?

A

-have a memory but also lot of facts surrounding it, = pulling one element then brings things associated with it.

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7
Q

What is a characteristic of explicit memory?

A

-it is associative -related information is recalled together

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8
Q

What happens when you’re recalling a memory?

A

-Recall of stored memory of an event activates parts of cortex activated when the event was sensed – The event is partially relived

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9
Q

What is the role of the neocortex in memory?

A

-storage

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10
Q

What happens during long term memory formation?

A

-During long term memory formation (takes days) continual interaction between neocortex and hippocampus -after a while you don’t need the hippocampus to recall the memory,

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11
Q

How is memory stored?

A

-as strength of connections between neurons in a network

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12
Q

Is memory dependent on individual neurons?

A

-Individual neurons can participate in several memories -Distributed, rather than depending on single neurons -Usually located close to the region that responds to a specific modality

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13
Q

What is sparse coding?

A

-one neuron per memory not true, more neurons involved in one memory, can multiply the numbers of memories you can have

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14
Q

What is the structure of memory?

A

-this is not only for neurons -collection of neuron-like interconnected elements -when give a stimulus then all will be activated (the ones that are sensitive to it) -interactions between the neurons get stronger and stronger -consequence is when stop the training stimulus= but not they are strongly interconnected and activating one will activate the others -partial activation gives the complete original stimulus =associative memory -memory is a natural consequences of having neurons taht can change the connections between them in response to repeated stimuli

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15
Q

What is long term potentiation? (Hebbian modification)

A

Long term activity dependent plasticity that satisfies the criterion that synapses strengthen when pre- and post-synaptic neurons are active at the same time -Long term potentiation (LTP) -one neuron active at the same time as postsynaptic nerons= that strengthens the connection LTP -with repetition becomes a memory trace

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16
Q

What is long term depression?

A

-(LTP) is another form of Hebbian modification -where presynaptic and postsynaptic neuron are not active at the same time= then less connection! LTD

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17
Q

What is neuronal scaling?

A

LTP= even though synapse gets stringer, adjustment (neuornal homeostasis) to frequencies, so when the connection stronger the firing stronger but not that much neuronal scaling= brings the synapses to appropriate level, so the connection not too strong

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18
Q

How is LTD self-regulated?

A

-LTD= is self regulating, eventually will stop working if too strong (as no connection)

19
Q

What does the strengthening of synapses occur via?

A

-via long term potentiation (LTP)

20
Q

What does the weakening of synapses occur via?

A

-occurs via long term depression (LTD)

21
Q

What do we need for true long term effect (memory)?

A

-protein synthesis -you need to alter the synapse permanently to get a long term memory -if block protein synthesis then no memories formed -point of LTP and LTD is to set up the system to have the long term changes in synapse (protein synthesis)

22
Q

What does this picture show?

A

-LTP -frequency is the test -tetanus= high frequency stimulation is applied to the axon 1, the size of the output is increased after this -the effect lasts for up to a month =if put the same input to input 2 then not increased -the neuron remembers that only input 1 was stimulated

23
Q

What does this picture show?

A

-LTD -give stimulus that is not strong enough to activate the neuron -then the response gets smaller, this effect lasts long = LTD -remembers that this input is ineffective -the other set of inputs doesn’t get activated -associated already

24
Q

Why is it easier to form new memories in the hippocampus?

A

in hippocampus= the changes not as constant in absence of stimulation, so can form new memories more easily in neocortex (the LTD and LTP)

25
Q

How long does facilitation and depression last?

A

-temporary things (millisecond in facilitation, seconds in depression)

26
Q

What is the postsynaptic mechanism for LTP?

A

1.-glutamate excited AMPA receptors (Na+ going in) 2.-the depolarisation unblocks NMDA receptors 3.-Ca2+ going in through the NMDA 4.-Ca2+ activates dependent kinases 5.-the kinases phosphorylate AMPA receptors or cause insertion of AMPA receptors into the terminal membrane -thus the cell is more easily excited by glutamate now -more activation -happens on the postsynaptic terminal on synaptic spines

27
Q

How are NMDA receptors blocked?

A

-by a Mg+ ion, it is unblocked by the excitation of AMPA receptors and the influx of Na+ ions

28
Q

Where is the Ca2+ during the LTP mechanism?

A

-in the dendritic spine not in the dendrite

29
Q

How can Ca2+ enter the cell in LTP mechanism?

A

-via NMDA receptors -also voltage gated Ca2+ channels

30
Q

Where is calcium-calmodulin dependent protein kinase II (CaMKII) found?

A

-in spine cytoplasm (of neurons) -associated in rings of 10 subunits -chemical memory!

31
Q

What disinhibits the CaMKII activity?

A

Ca2+ - calmodulin complex -activated when Ca2+ influx when NMDA receptors activated in LTP

32
Q

What happens to CaMKII when Ca2+ influx?

A

1.-normally the hinge like subunit of CaMKII is off 2. the hinge opens upon binding of Ca2+- bound calmodulin, freeing the catalytic region to add phosphate groups to other proteins 3.large elevation of Ca2+ can cause phosphorylation of one subunit by another (autophosphprylation) which enables the catalytic region to stay on permanently

33
Q

Where is calmodulin found and what can it do?

A

-found in the cytoplasm, when bound to calcium can modify fucntions of other things in cell

34
Q

What does phosphorylation of CaMKII do?

A

-Phosphorylation makes CaMKII constituitively active until dephosphorylated by a phosphatase

35
Q

How is memory stored in CaMKII?

A

-Memory stored in number of CaMKII molecules within ring that are phosphorylated

36
Q

What is one of the mechanism of protein synthesis in formation of long term memory?

A

-involves phosphorylation of CREB which regulates gene expression

37
Q

What is CREB?

A

-(cAMP response element-binding protein) is a cellular transcription factor. It binds to certain DNA sequences called cAMP response elements (CRE), thereby increasing or decreasing the transcription of the downstream genes

38
Q

What opens the Ca2+ voltage gated channels? (in LTP)

A

-Back-propagating dendritic action potentials can open voltage-dependent Ca channels

39
Q

How can you also increase the cytoplasmic Ca2+ ?

A

-Can also increase cytoplasmic Ca2+ via release from intracellular stores – e.g. the metabotropic glutamate receptor mGluR1 causes Ca2+ release from endoplasmic reticulum

40
Q

What is the sum of Ca2+ entry via NMDA and voltage-dependent channels?

A

Ca2+ entry via NMDA plus voltage-dependent channels greater than sum of separate routes of entry by themselves

41
Q

Why is the timing of Ca2+ entry key?

A

-Ca2+ is needed for both LTD and LTP= which one it is, is dependent on the amount

42
Q

When do we have an LTD? (spike timing plasticity)

A

When action potential in post-synaptic neuron occurs before an EPSP total increase in Ca2+i is small – Activates Ca2+-dependent phophatase – LTD

43
Q

When do we have LTP? (spike timing plasticity)

A

When NMDA-receptor -mediated EPSP occurs before post-synaptic action potential increase in Ca2+i is much larger – Activates CaM Kinase II – LTP