Synaptic Transmission Flashcards
synapses
cell-to-cell communication occurs here
cells come in contact
-electrical synapse
-chemical synapse
electrical synapse
gap junction; connexons(6 per pore)
fastest; nearly simultaneous
bidirectional
synchronized signal; large neural network
interneurons, hormone secreting neurons in hypothalamus
chemical synapse
AP arrives, local increase in cytoplasmic Ca2+ -> synaptic vesicles fusion
neurotransmitter released into synaptic cleft
binds to specific receptor on postsynaptic cell
transmission sequence
transmitter stored in synaptic vesicle AP enter depolarization/Ca2+ channels open influx of Ca2+ synaptic vesicles fuse release transmitters transmitter diffuse across synaptic cleft transmitter binds to receptors ion channels open or close - PSC can be either excitatory(EPSP) or inhibitory(IPSP) vesicular membrane recycled
EPSP and IPSP
excitatory post synaptic potential
inhibitory post synaptic potential
Loewi’s experiment
chemical neurotransmission
ACh in mAChR - contraction slowed down; inhibitory
neurotransmitter criteria
- present within the presynaptic neuron; enzymes, precursors
* some needed for protein synthesis: glutamate, glycine, aspartate - released by depolaration and require Ca2+ influx
- receptors must be present on post synaptic cell
exogenous? agonist? Antagonist?
exogenous transmitters can mimic
agonists and antagonists can alter transmission
(synaptic transmission at ) neuromuscular junction
neuron stimulated -> muscle membrane potential occurs : EPP (end-plate potential)
large enough to evoke AP
MEPP
- fusion of one vesicle (quanta) releasing its NT
spontaneous changes in muscle membrane potential
miniature(<1mV) EPP(40-50mV); look similar when compared to subthreshold EPP; integer multiples of MEPP
can be blocked by drugs that block postsynaptic receptors
Freeze fracture analysis
to study quantal release of NT # of fusion vs. #of quanta
Role of Ca2+
AP not prevented when Na+ channel blocked
voltage gated Ca2+ channel
* cadmium (ca2+ channel blocker) blocks both pre- and post- synaptic current/depolarization
sufficient and necessary
Ca2+ sufficient?
microinjection of Ca2+ in presynaptic nerve terminals evoke release even when AP was not present
Ca2+ necessary?
Ca2+ buffer blocked depolarization in postsynaptic neuron
two types of transmitters
small molecule
peptides
small molecule neurotransmitters
synthesized in presynaptic terminals
enzymes made in soma trnsported by slowaxonal transport
precursor transported into the nerve terminal
synthesized and packaged into vesicles
* final steps of synthesis sometimes occurs in vesicle
small clear core vesicles
neuropeptide
precursors synthesized in cell body
transported by fast axonal transport; kinesins
in terminal, enzymes modify precursors to produce the neuropeptides
when released, diffused away and degraded( proteolyticm enzyme)
release of small molecule NT or neuropeptides
low frequency stimulation -> local increase of Ca2+ -> small molecule NT
high frequency stimulation -> more diffuse in Ca2+ concentration -> neuropeptide and small molecule NT released
synaptic vesicles resued
experiment: HRP-horseradish peroxidase
budding (endosome)->docking->priming (exocytosis) ->fusion->budding (endocytosis)
coating
clathrin triskelion vesicle recovered (endocytosis) Adaptor proteins AP-2 & AP-180 facilitate Dynamin; final pinching HSC-70, auxilin, synaptojanin: uncoat
vesicle docking
complex: synaptobrevin&syntaxin&SNAP-25
Ca2+ controled: synaptotagmin; evoke fusion
SNARE complex
synaptobrevin, syntaxin, snap-25
pull membranes together
Ca2+ binds to synaptotagmin
synaptotagmin catalyzes membrane fusion
LEMS
attacks presynaptic Ca2+ channels
Congenital myasthenic syndrome
impared vesicle recycling
Botulinum and tetanus toxins
clostridial toxin
affect SNARE proteins involved in vesicle fusion
Clostridial toxin
protease
tetanus toxin, botulinum toxin
cleave presynaptic SNARE proteins
