task 3 - consolidation, plasticity, and long-term potentiation Flashcards

1
Q

hebbian learning

A

→ the principle that learning inolves the strengthening the connections of coactive neurons; often stated as “neurons that fire together, wire together”

  • if neuron A and B fire often at the same time the synapses between them hould strengthen → wiring them together
  • increasing the probability that when neuron A fires so will neuron B

→ explains how repeated experiences can enhance the ability to recognize familiar stimuli

→ changing the connections between cortical neurons creates a pattern that makes repeated stimulus more likely to be recognized and distinguished from other stimuli

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2
Q

long-term potentiation

A

a process in that describes the long-lasting strengthening of synpases between neurons, which is believed to be a fundamental mechanism underlying learning and memory in the brain: occurs when two neurons are activated simultaneously, leading to an increase in the stength of the synaptic connection between them

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3
Q

long-term depression

A

synaptic transmission becomes less effective after neurons do not fire together

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4
Q

studies platicity between neurons

A

steps: measures the baseline → uses an eletrode to give a small pulse to see what happens in the postsynaptic neuron → gives large pulses → causes (mimics) the co-activation of the pre and postsynaptic neuron → back to the original pulse → see if there is an increased response in the postsynaptic neuron

  • can see a larger spiking rate post the electrode stimulus
  • response gets potentiated → synapses strengthened
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5
Q

tentanus stimulus

A

very strong stimulus added to the pre synapse (artificial)

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6
Q

late LTP

A
  • gene expression causing structural changes
    • in post synaptic neuron and pre synaptic neuron
  • more stimulation leads to LTP
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7
Q

how does LTP relate to EPSP

A
  • how many receptors are available
  • sodium molecules are available to enter
    • the more that enters the higher the action potential
  • more LT → more EPSP → more connections
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8
Q

function of baseline data

A

→ assess the increased EPSP slope

→ represents the initial level of EPSP slope before any experimental manipulation

→ establishes a point of comparison

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9
Q

synaptic plasticity

A

proteins form signaling cascades that allow neurons to adapt to the input they are getting → these cascades link activity with connectivity

  • there are so-called ‘immediate early genes’ (IEGs) that are expressed in reaction to calcium influx during neuronal activity
  • IEGs produce transcription factors (proteins) that control expression of other so-called ‘late genes’ (LGs)
  • LGs produce proteins that can lead to changes in synaptic connectivity
    • e.g. more neurotransmitter (presynaptically), more receptors (postsynaptically)
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10
Q

place fields

A

occurs in the hippocampus associated with memory and spatial navigation, refer to specific locations in an animal’s environment where a hippocampal neuron becomes active or fires

proved with the experiment as it shows the firing of the hippocampus in the rat as forming/taking in the environment

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11
Q

relevance for place cells → 2 main LTM theories

A

both theories discuss that the hippocampus helps to bind neurons together that are activated during an experience to form a memory trace

  • role in memory formation
  • binding role in memory (intial plasticity between cortical neurons and hippocampal neurons must happen very quickly after the experience
  • reactivates and then co-acticates neurons → turning them into a memory trace
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12
Q

place cells relevance to LTP

A

mutual involvement in the processes of learning and memory consolidation → within the contect of spatial memory

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13
Q

place cells relevance to LTP

spatial learning, synaptic plasticity, memory consolidation

A

spatial learning
- forming connections between neurpns representing different locations, undergoing LTP to strengthening the synaptic connections between them

synaptic plasticity
- necessary for encoding spatial memories

memory consolidation
- during exploration and learning the information is processed → LTP is a mechanism by which memories are encoding and consolidated in the hippocampus

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14
Q

EE paradigm

A
  • grater activity of enzyme AChE
  • thicker heavier cerebral cortex compared to IC
  • promotes better learning and problem solving
  • aids recovery
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15
Q

early LTP

A

more neurontransmitter, temporary receptors, more sensitive, depolarizes more easily, depolarizes easily, requires no genomic response

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16
Q

late LTP

A

more coactivation, more receptors are permanent, requires new protein synthesis, requires genomic response

17
Q

IEGs

A

‘immediate early genes’ (IEGs) that are expressed in reaction to calcium influx during neuronal activity

18
Q

late genes

A
  • IEGs produce transcription factors (proteins) that control expression of other so-called ‘late genes’ (LGs)
  • LGs produce proteins that can lead to changes in synaptic connectivity
    • e.g. more neurotransmitter (presynaptically), more receptors (postsynaptically)
19
Q

late LTP steps

A
  1. calcium molecule is activating calodulin
  2. calmodulin interacts with protein kinase C
  3. these two together bring more pre fabricated channels to the postsynaptic density
  4. the postsynpatic neuron is more sensitive for the same amount of glutamate→ more receptors means bigger EPSP
20
Q

early LTP

A
  1. glutamate releases
  2. glutamate binds to AMPA receptors -> influx of Na+ and depolarization
  3. once significantly depolarized Mg ions blocking NMDA are released -> glutamate activates -> influx of Ca+
  4. activates CamKII and PKC (protein kinase C)
  5. they will phorphorolyze AMPA receptors -> increase conduct and greater postsynaptic response to glutamate
  6. enhance synaptic strength by cam adding more AMPA receptors
21
Q

neuromodulators

A

neurotransmitters released by neurons in areas in brainstem

→ They can affect activity in entire brain areas and alter/modulate how neurons exchange messages, even if they themselves are not part of messages

22
Q

synaptic plasticity

A

synpases to changes as a result of experience

Neurons can change physically, as a result of learning – These changes affect how neurons communicate and how brain systems function.

23
Q

LTP - Changes in presynaptic neuron

A

Retrograde messenger can be released by post-neuron, diffused across synapse to pre-neuron and can increase amount of NT is releases in future

24
Q

LTP to learning

A

a. Drugs that block LTP can impair animal’s ability to learn and;
b. Rats that have been genetically bred to have enhanced LTP, show better learning than normal rats.

25
Q

Physiological changes at synapses store information

A

a. Increase in size of postsynaptic receptor membrane causes larger response to same amount of transmitter release.
b. Interneuron modulates polarization of axon terminal and causes release of more transmitter molecules per nerve impulse.
- Interneurons modulate activity of presynaptic neuron and can influence co-activation and ensuing plastic changes. They use as neurotransmitter dopamine, noradrenaline and serotonin, which have been associated with reward signals, attention/arousal and mood regulation.

26
Q

Structural changes at synapse provide long-term storage

A

c. Neural circuit that is used more often increases number of synaptic contacts.
d. More frequently used neural pathway takes over synaptic sites formerly occupied by less active competitor.

27
Q

Dual-trace hypothesis

A

Formation of a memory, first involves a brief transient process, in which learning experience sets up activity that tends to repeat through activated neural circuits. Then, this activity holds memory for short period and if activity is sufficient, it helps build up stable change in nervous system, a long-lasting memory trace

28
Q

CA1 region

A

Hippocampus has several regions and one of them is CA1, which as two kinds of glutamate receptors

29
Q
  1. AMPA receptors
A

Bind glutamate agonist → Glutamate first activates these receptors

30
Q

NMDA receptors

A

Selective ligand → Do not respond until enough AMPA receptors are stimulated, and neuron is partially depolarized

31
Q

cellular consolidation 2 steps

A
  1. Synaptic transmission between two coactive neurons becomes more efficient → Not permanent and wears off after some hours.
  2. For long-term memory, synaptic changes that would underlie formation of new memory trace, would have to be more stable and long-lasting → If we can create conditions in which two cells are co-activated multiple times, the resulting increase in synaptic strength becomes more permanent
32
Q

relationship between genes and long-term plasticity

A

A requirement is that gene expression that leads to neuronal modification is under co-activation.
=> Depending on the cells and brain structures involved, long-lasting plasticity can depend on pre-or postsynaptic plasticity, or both.
=> Without sensory experience, there will be no co-activation and thus no new memory.
=> How well memory formation process will be executed depends on presence and activity of all necessary genes. N.B.: LTP is not equal to plasticity