Synaptic plasticity LTD n LTP 26/11 Flashcards

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1
Q

What is the name of the structure of where neurons communicate?

A

Synapses

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2
Q

What causes the release of neurotransmitters into the synapse?

A

Action potential coming down from axon into axon terminal

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3
Q

What is a post synaptic density region?

(3 marks)

A
  • Electron dense structure that is positioned after the synaptic cleft
  • Keeps shape of spine of synapses
  • Anchors/ keeps receptors in synaptic zone
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4
Q

What is Hebb’s postulate?

(2 marks)

A
  • When axon of cell A is near enough to excite cell B it takes part in firing it repeatedly
  • Growth processes or metabolic change takes place in one or both cells such that A’s efficiency as one of the cells firing B is increased
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5
Q

What is Hebb’s learning rule? (explanation of his postulate)

(2 marks)

A
  1. Correlated pre and post synaptic activities cause synapse strengthening and stabilization by action potential coming down axon to post synaptic neuron - this may be the basis of information storage
  2. Uncorrelated activity between synaptic partners would weaken the connection - cells that fire together wire together
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6
Q

What is an action potential?

A

Large, brief depolarisation of the membrane potential - unit of transmission

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7
Q

What is ‘synaptic potential’?

A

Depolarizing or hyperpolarising potentials due to activation of NT receptors . Many receptors on post-synaptic membrane are ionotropic causing change in potential

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8
Q

What is an EPSP?

A

Excitatory post synaptic potential - current measure of strength of synapse

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9
Q

What can many EPSPs do together?

A

Summate together - lots of AP coming in at onetime on same neuron and if big enough can fire action potential

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10
Q

Which brain structure was LTP first found in?

A

Hippocampus

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11
Q

Why is the hippocampus the chosen area to study LTP?

(4 marks)

A

Highly laminus structure with 3 interlocked sheets:

  1. Cells in dendate gyrus - glutamatergic excitatory cells
  2. CA3 pyramidal cells - connected by 3 different pathways
  3. CA1 region - all dendrites in laminus structure
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12
Q

How are the 3 groups of cells in the hippocampus connected?

What pathways are involved?

(4 marks)

A
  • Perforant pathway from the entorhinal cortex - axons from here join onto dentate granule cells
  • Dentate granule cells send fibres in mossy fibre pathway
  • ^^axons infringe on dendrites of CA3 cells
  • CA3 cells infringe in bundle called Schaffer collateral and bind to CA1 cells
  • From this can make recordings in post synaptic cells
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13
Q

Explain how the results were generated in this image.

(7 marks)

A
  • Signal given to stimulate perforant pathway and then measured EPSPs
  • Plotted max amplitude of deflection from the max response
  • Given pathway a high frequency stimulation at 0 mins at 100hz per second
  • ^^ known as Tetanus - train of bursts
  • Rapidly see bigger change in response in EPSPS
  • Bigger response for every stimulation they do after they’ve given brief high frequency stimulation than before
  • Provided first evidence that nunch of synapses can change in response to an activity after stimulation
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14
Q

What are th 2 phases LTP is divided into?

(2 marks)

A

Induction: occurs during brief tetanus

Expression: way in which synapses are altered after LTP

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15
Q

What is input specifity?

A

LTP only occured in tetanized pathway

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16
Q

What is cooperativity?

(2 marks)

A
  • Weak input in which only few excitatory synapses were tetanized, failed to induce LTP, whereas a strong input reliably produced LTP
  • Weak induction - only few synapses will be active - causes few seconds of potenciation
17
Q

What is associativity?

A
  • Simultaneous activation of 2 seperate synapses, one of which is weak and fails to undergo LTP on its own but is able to exhibit LTP and potenciation when tetanized together with a strong input
18
Q

What can prevent LTP?

(2 marks)

A

Hyperpolarisation - shows LTP has 2 requirements of LTP: synaptic stimulation and post synaptic depolarisation

19
Q

What receptors is excitatory neural transmission dependent on?

A

NMDA & AMPA receptors - LTP critically dependent on activation of NMDA receptors

20
Q

Describe in detail what are NMDA receptors?

(6 marks)

A
  • Multimeric ion channel
  • Ionotropic receptors
  • Binds glutamate
  • Co-agonist glycine binds to receptor but ions won’t flow in
  • Mg2+ blocks pore unless depolarised
  • Are ligand and voltage gated calcium permeable receptors NMDA
21
Q

How can you remove the block of Mg2+ on NMDA receptor?

(4 marks)

A
  • By binding glutamate
  • Opens NMDA receptor (unless membrane sufficiently depolarised)
  • Relieving Mg2+ block and receptor lets in Na+ and Ca2+
  • Influx of Ca2+ improtant for induction of LTP
22
Q

Why is the influx of Ca2+ important for LTD?

(2 marks)

A
  • Causes activation of CamKII
  • Can increase AMPA insertion into dendritic spine and also in some forms of LTD and see w/ drawal of AMPA receptors
23
Q

What are two mechanisms that are also responsible for long-lasting potentiation?

(2 marks)

A
  • Increase in efficiency of synaptic transmission at perforant pathways
  • Increase in the excitabliilty of granule cell population