L5 Synaptic basis of neuroplasticity
11 important questions on L5 Synaptic basis of neuroplasticity
On which kind of neuron are AMPA and NMDA receptors found? Inhibitory or excitatory?
Identity of neurons is not about the receptors they express but about the neurotransmitters they release.
What is the result on the plasticity by over-expression of NMDA receptors?
What is Long term synaptic potentiation (LTP)?
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Which of the following is NOT a common feature of LTP in the CNS?
1. LTP can persist for months in vivo
2. Induction but not maintenance of LTP requires gene translation
3. Maintenance but not induction of LTP requires gene transcription
4. Strong stimulation induces long-lasting potentiation
5. Weak stimulation induces short-lasting potentiation
2, 3
Feature:
1, 4, 5
note: induction but not maintenance of LTP requires gene transcription; maintenance but not induction of LTP requires gene translation
induction LTP -> gene transcription
Maintenance LTP -> gene translation
(zelfde aantal i'tjes)
What are the four step in induction of the Long-term synaptic potentiation ?
- Activation of NMDA receptors
- Increased postsynaptic calcium
- Activation of CaMKII
- Enhancement of AMPA receptor function
What are two forms of long-term synaptic plasticity?
- Physiological: Change in the efficacy of synaptic connectivity
- Best studied in vitro brain slices using electrophysiological methods
- Relevant amount of change in long-term efficacy (long-term potentiation (LTP) vs Long-depression (LTD)) is a direct measure of synaptic strength.
- Anatomical: Addition and removal of synaptic connections between neurons
- Best studied in vivo, in intact brain circuits by longitudinally visualising synaptic connections
- Change in the synaptic count, shape of synapses, turnover rate and motility reveal anatomical nature of synaptic connectivity
It is generally accepted that a synapse should first express physiological plasticity to express anatomical changes.
What is the central dogma of synaptic plasticity? (Donald Hebb 1849)
Neurons that fire together wire together.
means the more you run a neural-circuit in your brain, the stronger that circuit becomes. ... The more you practice piano, or speaking a language, or juggling, the stronger those circuits get. Scientists have known this for years.
In other words, the simultaneous activation of neurons strengthens the connection between them
What mechanism could mediate synapse specificity of plasticity?
- tags
What does postsynaptic injection of active CaMKII fragment potentiate?
What are methods for conditional up-regulation of LTP - making a smarter mouse
- Over-express NMDA receptors - improve LTP and spatial memory (on Morris Water Maze)
- Inhibit Calcineurin (is phosphatase) - should improve LTP and spatial learning performance (on the Morris Water Maze)
The molecular mechanisms of NMDA mediated enhancement of LTP
- Over-express NMDAR
- when the intracellular calcium concentration rises moderately
- A phosphate "Gate" modulates CaMKII signaling
- the gate is controlled by cyclic AMP
- Blocking PKA should reduce LTP as increased intracellular calcium will no longer inactivate PP1a action (so PP1a must be inactive for LTP)
- LTP is blocked by a PKA inhibitor and rescued by active inhibitor-1
- If the Gate is held open by directly activating the cAMP pathway
- If the Gate is held open by directly activating the cAMP pathway... Even weak stimulation induces LTP
- should improve LTP
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