NERVOUS SYSTEM: HEBBIAN AND SYNAPTIC PLASTICITY Flashcards

1
Q

define: synaptic plasticity

A

Synaptic plasticity: synapses can be modified to strengthen or weaken their connections and communications between them

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2
Q

State Hebb’s rule

A

Hebb’s rule: neurons that fire together are wired together; Outlines the basic principle that learning and memory can occur due to changes in the strength of connections between neurons

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3
Q

State the 2 physiological mechanisms for Hebbian principles

A

2 physiological mechanisms for Hebbian principles:
1. Long-term potentiation (LTP)
2. Long-term depression (LTD)

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4
Q

Define: homeostatic plasticity

A

Homeostatic plasticity: moves neurons back to their original state (set point) after modification of input

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5
Q

Define: facilitation/potentiation

A

in the presynaptic neuron, if the # of stimulation/s increases, EPSPs size increases

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6
Q

Define: synaptic depression

A

reduction in size of stimulation/s and EPSP size

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7
Q

Describe the trisynaptic circuit in the hippocampus; what is the hippocampus important for?

A

Input from entorhinal cortex → granule cell → granule cell input → CA3 → CA3 input → CA1

Important for making new memories

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8
Q

Define: long term potentiation

A

repetitive activation of an afferent pathway to the hippocampus or an intrinsic connecting increases the response of pyramidal cells; this can last for hours, days, or weeks depending on the system

Involves the modification of presynaptic and postsynaptic events

When stimulated at low frequency, EPSPs amplitude stays constant.
- When stimulated at high frequency for a short period of time, EPSPs after the period of high stimulation has a higher amplitude but slowly returns to baseline.

can operate through intracellular Ca2+ signalling; often dependent on glutaminergic receptors (AMPA/NMDA) and indicates structural changes in the postsynaptic terminal

-

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9
Q

What are 2 theories for why LTP occur?

A

What are some theories for why LTP occur?
- Presynaptic neuron is releasing more neurotransmitter
- Or; same neurotransmitter release but more post-synaptic receptors (the most favoured theory)

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10
Q

Describe postsynaptic events that lead to an Increase in AMPAR during LTP

A

LTP: With much stronger depolarization, you will get more release of glutamate and a large depolarization. Mg2+ is removed from NMDA which allows for Na+, K+ and Ca2+ flux. Ca2+ influx through NMDA activates intracellular CaMKII pathway which causes AMPAR phosphorylation and insertion of more AMPA receptors in postsynaptic membrane from vesicles

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11
Q

For AMPA
- give full name
- give receptor type
- what is it permeable to?
- describe what kind of current it has at negative mV and at positive mV

A
  • a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid
  • glutamate receptor
  • Permeable to Na+ and K+
  • Inward current at negative mV, positive current at positive mV
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12
Q

For NMDA
- give full name
- give receptor type
- what blocks it? how can it be unblocked
- what is it permeable to?
- describe what kind of current it has at negative mV and at positive mV

A
  • N-methyl-D-aspartate
  • glutamate receptor
  • At resting membrane potential, NMDA receptor is blocked by Mg2+; Depolarization dispels Mg2+
  • Permeable to Na+, K+ and Ca2+
  • at negative mV, no current until Mg2+ is dispelled which occurs at -60 mV. inward current until at positive mV then it is an outward current
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13
Q

Describe postsynaptic events that lead to an decrease in AMPAR during LTD

A

LTD: With weak depolarization, you have short term decreases in EPSPS caused by inactivation of Cav channels or depletion of neurotransmitter-containing vesicles. This results in the
activation of phosphatases (protein phosphatase 1 - PP1 and calcineurin) that act on AMPA which results in the internalization of AMPA receptors

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14
Q

What will bilateral loss of hippocampi result in?

A

anterograde amnesia - inability to form new memories

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15
Q

Describe the 4 major structures that form the neural circuit inthe hippocampus

A
  1. CA1: major output goes to layer V of the entorhinal cortex (EC)
  2. CA3: receives input from the dentate gyrus (DG) and from the EC
  3. DG - dentate gyrus : projects to CA3 and receives input from the EC
  4. EC - entorhinal cortex (MTL): an interface between the hippocampus and the cortex
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16
Q

What will repeated stimulation of entorhinal cells that project to dentate gyrus result in?

A

Repeated stimulation of entorhinal cortex cells that project to dentate gyrus leads to increased EPSPs in dentate gyrus over time, consistent with Hebbian principles

17
Q

What is meant when it is said that the 2 principles for hippocampal LTP are:

  1. input sensitivity
  2. cooperativity
A
  1. Input specificity: only the activated set of synapses will be potentiated
  2. Cooperativity: enough presynaptic axons must fire coincidentally to activate the postsynaptic cell
18
Q

Define: dendritic spine

A

little bumps on the dendrites where you have a lot of synaptic input from other excitatory inputs

19
Q

How do the dendritic spines change with strong depolarization (as with LTP protocol)?

A

Dendritic spines can become more prominent.

20
Q

Define: long term depression

A

Weak activation of presynaptic neuron –> weak depolarization and little Ca2+ influx

activates phosphates that dephosphorylate AMPARs promoting receptor endocytosis

21
Q

define: localization

A

localization: ascribes particular functions to particular regions or groups of neurons

22
Q

define: connectionsim

A

Connectionism: ascribes functions to connections between neurons, and Hebbian plasticity provides a connectionist account of learning, memory and development

23
Q

1 day after learning, where are associations the strongest? What about 36 days after learning?

A

1 day after learning, most associations involve hippocampus
36 days after learning, connections more strongly involve cerebral cortex, thalamus

Explains why loss of hippocampus prevents new memories, but old memories remain intact