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Action potential and propagation - Coggle Diagram
Action potential and propagation
iput: EPSCs and IPSCs
affected by passive properties (R, C, constants
length constant
lamda = sqrt(rm / ri) = sqrt(aRm / 2Ri)
m--membrane
i--axial
length constant should be sqrt(rm / ri +ro )
o--extracellular resistance
but extracellular resistance would be negligible
time constant
taum = rmcm = RmCm
computation/integration
EPSP/IPSP summation
spatial
input come at the same time in different location
depends on suitable length constant so input wont degrade before summation
temporal
input come at the some location but differrent time
depend on time constant
output: AP
AP generation
axon hillock (the first part of axon initial segment
why? the distribution of low threshold sodium channel Nav1.6 are mainly in axon hillock, while the high threshold Nav1.2 in the soma
conduction
with myelin
saltatory, determined by active properties voltage gated ion channels
all or none property
back propagation will nor regenerate AP in axon because of refractory period
signals in soma does not depend on potassium channel because its not AP but back propagation or summation.
AP is reshaped by Kv channel in the axon
exception: CA3 pyramidal cell has active dendrite conduction
hypothesis
block information coming from the other side
feedback loop--neuron can activate itself
mechanics
sodium spikes
calcium spikes
fast kinetics, threshold not low
involve in bursting of neuron, can largely depolarize soma and happen many times
NMDA spikes
propagation failure
branch point
thicker axon are more prone to have failures ( so branch can be viewed as frequency filter
propagation reflection
full conduction
the minor field stimulation evades the whole axonal arborization
reflection
slightly hyperpolarized cell
the reflection from 1 position enhance transmission from other position
conduction block
hyperpolarized cell
conduction block lead to propagation failure
depending on the membrane potential of the presynaptic neuron, conduction, reflection and conduction block occur
chemical synapse
AP invade synapse
voltage-gated calcium channel open, calcium influx
vesicle fuse with membrane
NTM release
bind with pre-/post-/peri-/extrasynaptic receptor
uptake by glia (mostly astrocytes
enzymatic degradation
recycling by presynaptic neuron
synaptic short-term plasticity
depression
facilitation
facilitation and depression
short-term synaptic dynamics is synapse specific
main factor: residual Ca2+
long-term plasticity
spike-timing dependent plasticity
exception
electric sensor of electric fish
GABAergic neurons in hippocampus
neo cortex-layer 4 spiny stellates
also depend on the synapse location (not likely terminal
LTP mechanism (glutamate
ca influx from NMDA receptor activate calmodulin affect
calmodulin kinase
increase AMPA receptor
PKC
#
tyrosine kinase
#
generate retrograde signal NO
enhance NTM release
gene transcription