13- Synaptic physio lab Flashcards
visually observed transition from indiv muscle twitches to tetanus as the ____
frequency of stim to motor nerve is incr
events that cause transition from muscle twitch to tetanus with incr freq of motor n. stim
1) single AP causes NT release
2) post syn membrane depol
3) Ca2+ release from SR
4) @ high freq, muscle cell can’t remove all Ca so builds up
5) so can’t relax btwn contractions and muscle stays contracted
describe quantum hypothesis
Experimental observations underlying Quantum hypothesis of transmitter secretion
each secretion of NT occurs in integral # of multimolec packets (quanta)
small 1 mV depol at random intervals
stim of nerve –> large synch release of quanta
EPP proportional to # quanta release or summation of MEPP
Difference btwn MEPP and EPP
MEPP = small depol (~ 1 mV amplitude) from spont release of vesicle
EPP = caused by nerve stim with synch release of many vesicles (if large enough, can depol postsyn cell –> twitch)
Describe effects of bathing prep with curare
no MEPPs or evoked potentials even with high freq stim
Describe effects of bathing prep with elev Mg/low Ca
mimics the effect ____
MEPPs seen but evoked potentials can’t be seen until high freq stim (to cause facilitation)
Describe mechanism by which curare produces effects
blocks postsyn transmission by bind to nAChR so no MEPP or EPP
Describe mechanism by which high Mg/low Ca produces effects
mimics the effect of ____
pre-synaptic block since not enough Ca to allow NT release
Ca influx into cell is req’d for exocytosis
MEPP visible as not regul by Ca2+ release
mimics the effect of botulism
Effect of neostigmine on synaptic transmission
Neostigmine = AChE inhibitor so ACh prolonged in cleft
potentiates effects of ACh on incr in neurotransmission and incr muscle twitch
but neostigmine also similar strxr to ACh so overdose can cause to bind ACh receptor and antagonize
–> facilitation then depression @ high freq
Understand synaptic facilitation
of quanta secreted from terminal is larger b/c residual calcium allows exocytosis of more vesicles since can’t clear calcium fast enough
Understand synaptic facilitation in low Ca/high Mg solution
presynaptic block that prevents neurons from releasing NT (not enough Ca to cause exocytosis)
but high freq stim will cause Ca level to be high enough to release enough vesicles for twitch
Understand synaptic depression
depletion of releasable synaptic vesicles
repeated stim can’t replenish vesicles fast enough to keep pace so decr # of secreted quanta
Understand synaptic depression in curare solution
curare blocks nAChR
so muscle cells won’t respond to single or high freq stim because ACh can’t bind
Causes of myasthenia syndrome
Ab to pre-synaptic Ca channel
prevent influx of calcium
vesicles cannot fuse with membrane and NT cant be released
Symptoms of myasthenia syndrome
weak but get stronger with activity due to facilitation
continuous AP with activity incr Ca2+ in axon since not all Ca pumped out