Synaptic Plasticity Flashcards

1
Q

Santiago ramón y Cajal (1894) stated

A

memories might be formed by strengthening connections between neurons

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2
Q

Hebbs law =

A

when axon A is near enough to excite cell B and repeatedly takes part in firing it - some growth process or metabolic change takes place in one or both cells
A efficiency as one of the cells firing B is increased

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3
Q

when A and B fire AP at the same time

A

the connection / synapse between them becomes stronger

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4
Q

synaptic plasticity

A

The strength of synaptic communication between 2 neurons is not fixed
change in the strength of synaptic communications

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5
Q

how was long term potentiation first studied

A

recordings of fEPSP in performant pathway of rabbits
insert stimulating electrode into pathway
eject dendrite gyrus of hippocampus into dendritic field
record synaptic responses
experiments - change amplitude vs control

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6
Q

experiment to test hebbs law

A

evoke activity in A using stimulating electrode
see response in B
depolarisation of membrane potential to generate postsynaptic potential

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7
Q

general properties of LTP

A

input specificity
associativity
cooperatively
persistence

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8
Q

what is input specificity

A

LTP is induced selectively at a synapse or group of synapses that are formed between pre and post synaptic neuron
simultaneous activation of A and B - synapse between A and B is activated then this synapse will undergo LTP

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9
Q

what is associativity

A

a weak stimulus in one pathway is not sufficient to elicit LTP
when paired with activity in another strong pathway = LTP in both pathways

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10
Q

example of associativity (LTP)

A

A = weak
C = strong
if activity is just in A = B is not potentiated
is activity in A and C simultaneously = activity is elicited in B = both of the synaptic pathways undergo LTP

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11
Q

cooperatively if LTP

A

a weak stimulus in one pathway is not sufficient to elect LTP
when paired with another (does not have to be strong) pathway = LTP in both pathways

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12
Q

different between associativity and cooperatively

A

similar to associativity but does not require the second pathway to have a strong stimulus = just several input pathway activated at the same time

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13
Q

persistence LTP

A

increase in synaptic strength will last across time
after LTP occurred the AP is A will be more likely to drive an AP in its postsynaptic partner B

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14
Q

what is LTP induced by

A

high frequency conditioning stimulation

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15
Q

what receptors are required for LTP at a synapse

A

NMDA

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16
Q

why are NMDA receptors coincidence detectors

A

they detect presynaptic activity / glutamate
detect postsynaptic activity / depolarisation too

17
Q

when are NMDA receptors activated

A

depolarised potentials

18
Q

how are NMDA receptors blocked at polarised potentials

A

NMDA receptors
hyperpolarised/polarised potentials
magnesium ion blocks channel pore
prevents other ions moving across

19
Q

when glutamate binds to NMDA receptors

A

glutamate binds
magnesium ion block is removed
so now with glutamate ions can pads through channel pore into post synaptic cell

20
Q

what is needed to get LTP in NMDA receptors

A

Glutamate and depolarisation at the same time
= LTP

21
Q

why does NMDA receptors activation lead to LTP

A

allow calcium to enter
influence In facilitating LTPs

22
Q

why can’t AMPA activation lead to LTP

A

AMPA = allows movement of sodium ions
not calcium ions

23
Q

experiment of calcium on LTP

A

CA3 to CA1 synapses in hippocampus brain slices
EPSP
number of cells filled with calcium chelator (nitr5)
high frequency stimulus
cells filled with nitr5 = take up calcium - can’t undergo LYP
shows calcium is essential for LTP

24
Q

calcium effect on LTP

A

binding of calcium to calmodulin to CaMKII enzymes
causes a conformational change
active sites of the enzyme are released
able to go and act on downstream effectors

25
Q

what intracellular signalling cascades does calcium activate

A

ca2+/calmodulin kinase
protein kinase C
calpaan
G protein
adenylyl cycles

26
Q

what are the mechanisms by which LTP is expressed

A
  • change in release properties (presynaptic)
  • change in AMPAR properties (postsynaptic)
    *chnage in AMPAR numbers (postsynaptic)
    *synaptic growth (pre or post)
27
Q

what requires LTP to be induced in CA3 to CA1 synapses in hippocampus

A

Presynaptic glutamate release
Depolarisation of postsynaptic cell
Removal of the mg2+ block from NMDA receptors

28
Q

Long term depression

A

prolonged low frequency stimulation

29
Q

what do some forms of LTD depend on

A

NMDA receptor activation and Calum postsynaptic entry

30
Q

what can block LTD

A

intracellular calcium chelation using BAPTA

31
Q

LTD can be induced by

A

Activation of metabotropic glutamate receptors
activation of muscarinic ACh receptors

32
Q

3 processes involved in memory

A

encoding
consolidation
recall

33
Q

how do neuronal networks remember things

A

plasticity = enable strengthening of connections = information is now embedded in connectivity between the neurons involved in coding the stimulus
when the input is reactivated by a stimulus the activity is Abel to drive the reactivation of neurons with the network =beacuse of increase strength of connectivity

34
Q

too much LTP leads to

A

epilepsy

35
Q

too much LTP leads to

A

epilepsy

36
Q

LTP or LDP

A

HSF = NMDA receptor activation = LTP
LFS = NMDA receptor activation, MGLuR activation, mACh activation = LTD

different patterns of synaptic and NMDA receptor activation leads to different outcomes = LTP or LPD