Wikinotes

Maintainer: admin

synaptic plasticity:
- changes in strength of a connection based on recent firing patterns and modulatory transmitters
functions in
- learning and memory: experiences
- homeostasis : keep the overall excitability of a neuron
- mood and behaviour : alertness, different effect of the same stimuls at different time
strenght of a synapse(M) = NPQ
- P : probability of release of a synaptic vesicle after an action potential
- Q : amplitude of the post-synaptic potential (PSP) due to release of one vesicle
- N : number of synapses or vesicle release spots

amount of calcium
number of readily releasable vesicles
- readily releasable pool (RRP) can be measured with hypertonic shock with sucrose
- this would simultaneously fuse all primed vesicles -> can measure RRP
coupling of calcium entry to fusion of vesicles
also modulated by
- recent firing patterns -> paired pulse plasticity
- modulatory neurotransmission
  - ex: short-term facilitation in aplysia
- long-term potentiation
  - induced by PKA
  - have to do with Rab3A and phosphoryation of RIM

def: a change in probabilty of a vesicle fusing when two action potentials occur in succession
depends on the time in between pulses
due to residual calcium
- saturate the endogenous calcium buffers to that new calcium entering shortly afterwards gives rise to a higher concentration.
Types (not memory formation, because transient)
- paired pulse facilitation
  - second postsynpatic action potential is stronger than the first
  - if p was small for the first action potential
- paire pulse depression
  - second postsynpatic action potential is weaker than the first
  - if p was large for the first action potential ; more RRP was secreted
    - not enough time to regenerate the vesicles,
- post-tetanic potentiation
  - tetanic: high freqency action potential
  - will get depression first
  - wait a few minutes and then fire action potential : get facilitation
  - after short burst of action potential, there's an increase in p because:
    - residual calcium binds to calcium sensors
    - residual calcium persists because they can leak out of mitochondria after being reuptake

Munc 13 : calcium dependent increase in RRP :
- not only remove inhibitory effect of Munc18 on Syntaxin
- but also binds to calmodulin, a calcium senseor
- when the calmodulin-binding domain is removed, PTP is reduced
  - no calcium-induced increase in RRP
Unc 13
- regultory hub for priming
- DAG, produced by phospholipase C, directly binds to unc13
  - in combination of PKC phosphorylatino of Munc18 increase priming
- removing C1 domain of unc13 blocks modulation by DAG

aplysia, a stupid sea animal, can learn to retract its siphon faster after bieng shock
sensitization is due to serotoninergic interneuron
- serotonin increase synaptic strength in both motor and sensory neurons
repeated firing leads to less release and decrease of EPSP to motor neuron
- RRP is intact
- depression blocks calcium-secretion coupling
whereas, shock removes the desensitization/depression
- serotonin leads to more release and increase of EPSP to motor neurons
- does this by PKC regulation

shock release serotonin (5-HT) from interneuron
5-HT acts through G proein linked receptor and thereby increases cAMP level
cAMP activates PKA
PKA phosphorylates K+ channels and thereby inactivates them
- also increases priming in vertebrates via phosphorylation of RIM
slow repoloarization -> broadened action potential -> more calcium influx -> more transmitter - > bigger EPSP

seen at
- dentate gyrus to CA3
- parallel fibers to purkinje cells
- both depends on PKA activation
  - phosphorylates RIM and K+ channels
- both are gone in Rab3A or RIM knockouts
experiment on RIM
- replaces phosphorylated site with other amino acids
- lack of rescue with phosphorylation suggest phosphorylation of RIM is critical for LTP

need to know :
- M=NPQ
- PPF and PTP mechanism, how they relate to p
- sensitization and associative memories with the changes in p

Tuesday, March 25, 2014
Synaptic plasticity