L6 Flashcards

1
Q

describe Atkinson and Shiffrin’s model of memory

A

the first 300ms is sensory information

if that sensory information is attended then it goes into your short term memory (20 sec)

if this is reherced then it will go into long term memory

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2
Q

what is distributor processing

A

Distributor processing is storing information across multiple neurons

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3
Q

what is a cell assembly

A

particular pattern of activity in a group of interconnected

neurons

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4
Q

Each psychologically significant event, sensation, percept, expectation, memory or thought is the result of what

A

a cell assembly

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5
Q

what happens during the perception of an event

A

When you are perceiving an event, it corresponds to particular neurons cell assemblies that are becoming active

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6
Q

when something is in your short term memory, what is happening

A

Reverberating neural activity in closed-loop circuitry

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7
Q

why do we not store out memories in the way that we store short term memories

A

because the circuit needs to be active all the time you would run out of neurons and it would also be metabolically expensive

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8
Q

what is long term memory

A

Long term is when you strengthen the connections between neurons responsible for that particular experience

stronger synapse happen after consolidation meaning that those neurons have an increased potential for activation

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9
Q

how you you recall a memory

A

you activate the network from when you perceived the event that was that memory

the reactivation of this assembly occurs because of differential synaptic strength

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10
Q

what are Hebbs rules for whether a synaptic connection would strengthened or not

A
  1. when neurons fire you strengthen the connection which tends to induce lasting cellular changes that add to its stability (what happens)
  2. When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased. (how it happens)
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11
Q

what is Hebbian learning

A

When the postsynaptic and the presynaptic cell fire together then the connection between
them is strengthened

(cells that fire together, wire together).

Importantly, this allows for the association of inputs

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12
Q

what is the function of the amygdala

A

to produce an emotional response

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13
Q

explain how Hebbian learning allows for association of inputs

A

eg pain has a strong synapse to a neuron that causes you to feel fear.

when you are walking down the beach you see a crab. the neuron activated when you see a carb has a weak synapse to the neuron that causes fear therefore the action potential is not propagated.

however if the crab pinches you both the carb and the pain neuron are going to be activated at the same time and the weak synapse will become stronger

this means that the next time you walk down the beach and you see a crab, the synapse has become stronger so now you the AP will be propogated and you will feel fear

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14
Q

what is long term potentiation (LTP)

A

the strength of connections which last a long period of time

the bigger the strength of the EPSP the stronger the connection

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15
Q

why does long term potentiation suggest how memory works

A

you have a phenomenon which can strengthen synapses for a year (or possibly more)

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16
Q

does LTP have Hebbian properties

A

yes

specific to the pathways that are activated

This allows the nervous system to be very selective and gives you trillions of synapses which can be changed

17
Q

what receptors are on the postsynaptic neuron that allow for LTP

A

AMPA subtype of glutamate receptor and NMDA subtype of glutamate receptor

18
Q

describe the LTP induction mechanism

A

when glutamate binds to the AMPA receptor it lets Na+ into the cell causing depolerisation of the membrane

Sufficient depolarisation of membrane leads to unblocking of the NMDA channel

Calcium influx leads to LTP induction via downstream changes which increases receptors and then changes protein synthesis that
can induce long-term alterations in the strength of the synapse

19
Q

describe the AMPA receptor

A

when glutamate binds it lets Na into the cell

20
Q

describe the NMDA receptor

A

the NMDA receptor has a Mg2+ gate

Sufficient depolarisation of membrane leads to unblocking of channel because the inside becomes more positive pushing the +ive charge of the Mg gate out of the way

when this happens and glutamate is bound Ca can enter the cell

21
Q

what is the critical aspect of the LTP mechanism

A

it requires a conjunction of presynaptic and postsynaptic activity (Hebbian synapse)

You need a significant depolerisation to get the Mg out of the pore so Ca can get in

This can happen from one big input or lots of small ones

22
Q

how could you test to see whether LTP has anything to do with memory

A

Show that blocking LTP prevents memory formation

Show that reversal of LTP produces forgetting

Show that learning leads to LTP-like changes

Show that producing LTP creates false memories or masks existing memories

23
Q

what is an antagonist of the NMDA receptor

A

AP5

24
Q

how does AP5 effect LTP

A

you need the NMDA receptor for LTPs to occur therefore if the receptor is not working than LTPs cant happen

This is a dose dependent response

25
Q

what is the Morris water maze

A

it is a test for memory

it consists of a pool of water with a platform placed in a specific location just under the water so the rats cant see it

a rat is then placed in the water and they swim around until they find the platform. they learn very quickly where the platform is

you would then take the platform out of the water and if the rat spends more time swimming around where the platform was then it shows that they are looking for the platform and they have formed a memory of where the platform was

26
Q

how could you test to see if AP5 had an effect on memory using the morris water maze

A

you have a control group and then groups where the dose increases

you find that as the dose increases the time spent in each 1/4 of the pool balances out showing that with very high doses of AP5 that the animal never learns where the platform is

27
Q

LTP maintenance is dependent on….

A

protein kinase M zeta (PKMz)

28
Q

what dose ZIP (Zeta-Inhibitory Peptide) do

A

it inhibbits PKMz

this reverses the maintenance of late-phase LTP in vivo (it turns off LTP)

this means that when zip is injected the animal forgets what it has learnt

29
Q

what does zip show

A

it shows that when a normal action potential is fired there is no change but when zip is injected it dramatically decreases the baseline for EPSP

30
Q

what does protein kinase M zeta (PKMz) inhibition cause

A

PKM ζ inhibition abolishes long-term retention of spatial information

31
Q

what does 2 photon microscopy allow for

A

the imaging of tissue within a band 1 micron thick and at depths of up to 1 mm inside the brain

32
Q

when you are looking at a 2 photon microscopy image of a dendrite what are the fuzzy things

A

dendritic spines

this is where the axon terminals connect to the dendrite

33
Q

dendritic spine formation can be blocked by which NMDA antagonist

A

MK-801

34
Q

why is it important that the number of dendritic spines (connections) are regulated

A

As you learn more and more information you get more and more strong synapses

This could be dangerous as this is what happens in epilepsie

Also if this is the case what happens if the brain becomes full

35
Q

what is synaptic scaling

A

it is a form of homeostasis

This means that there is a continuous process in cell where when you strengthen some synapses you weaken others