NAS WK 1 - Action Potentials Flashcards
NAME COMMON NEURO-CONDITIONS
stroke, dementia, epilepsy, migraine
HOW NEURONES ARE LINKED
- terminals of one neurone adjacent to dendrite of other
- neurotransmitter (in synaptic vesicles) released into synaptic cleft to diffuse to dendrite (each dendrite has lots of synapses)
TYPES OF ION CHANNELS IN MEMBRANE
- non gated (set Em of resting membrane)
- gated (generate AP)
HOW -65MV MEMBRANE POTENTIAL MAINTAINED
- non-gated ion channels are more permeable to K+ efflux than NA+ influx so potential is negative
- Em remains constant though, NA+ influx must be equal to K+ efflux (as still -65) so NA+ driving force is larger than K+ but membrane is more permeable to K+ so balances out
WHY CONC GRADIENT IN MEMBRANE CONSTANT
changes in conc. are extremely small as number of ions moving is so tiny
ELECTROCHEMICAL FORCE
net force resulting from chemical & electrical influences
TRUE ROLE OF NA+/K+ PUMP
- doesn’t actually maintain the Em (-65mV) it just maintains conc. Gradients by 3NA+ out & 2K+ in (opp. to normal as opposes to even the conc.)but the actual Em is only maintained by movement of ions through the non-gated ion channels not the pump
- They don’t control Em they are only there because over long time periods the constant efflux of K+ would lead to vast changes in conc. So these are just there to stop that happening.
ION CHANNEL CONDUCTANCE (G)
- Gk = conductivity of K+ channel
- G(Na) = conductivity of NA+ channel
- G is proportional to number of open ion channels so change in conduction for ion = change in membrane potential
SUMMARY OF AP
Summary of AP
- Initial stimulus (depolarisation) opens the v-gated NA+ channels (increase in G(NA)) THEREFORE NA+ entry= further depolarisation & this further depolarisation leads to even higher G(NA) so membrane potential approaches NA equilibrium potential (as permeability of NA channel during AP = 1000x permeability at rest)
- NA+ channels inactivate (lower Na conductivity) so NA+ influx starts
- V-gated K+ channels open (higher Gk) & K+ leaves so repolarisation BUT the Gk remains high after membrane potential returns to rest THEREFORE Em approaches potassium equilibrium potential (hyperpolarisation)
- V-gated K+ channels close (lower Gk) so leak channels return the Em to resting value
EQUILIBRIUM POTENTIAL
ion is in equilibrium when chemical gradient & electrical forces are in balance
ABSOLUTE REFRACTORY PERIOD
- no more AP formed by stimulus (stops neurone releasing too many AP consistently)
- most Na+ channels inactivated but many K+ remain open so Na+ influx < K+ efflux (no depolarisation)
RELATIVE REFRACTORY PERIOD
- AP only form if stimulus is very strong (higher threshold needed as more Na+ channels need to open)
- Na+ recovering from inactivation & some K+ still open so it is possible but unlikely for Na+ > K+ (depolarisation)
AP MOVEMENT ALONG UNMYELINATED AXON (ELECTROTONIC SPREAD)
IN AXON, AP starts at one end then spreads along membrane as depolarises one end so opens Na+ channel which leads to adjacent Na+ opening so more depolarisation & this just repeats along axon
AP MOVEMENT ALONG MYELINATED AXON (SALTATORY CONDUCTION)
quicker as AP jumps between nodes of ranvier (gaps between myelin sheaths) so no need to depolarise whole axon (just jumps from + to - in nodes of ranvier)
WHAT FACTORS AFFECT SPEED OF CONDUCTION
myelination, larger axon diameter & higher temperature all increase speed of AP