S. Mochida et al., IMPAIRMENT OF SYNTAXIN BY BOTULINUM NEUROTOXIN C-1 OR ANTIBODIES INHIBITS ACETYLCHOLINE-RELEASE BUT NOT CA2+ CHANNEL ACTIVITY, Neuroscience, 65(3), 1995, pp. 905-915
The involvement of syntaxin, an omega-conotoxin-sensitive Ca2+ channel
-associated protein, in acetylcholine release was studied at synapses
formed between rat sympathetic neurons in culture. Transmission at the
se synapses involved omega-conotoxin-sensitive Ca2+ channels because a
dose-dependent inhibition was observed when omega-conotoxin was bath-
applied. Confocal microscope examination of immunofluorescent staining
showed that syntaxin had a similar distribution to synaptic vesicle-a
ssociated membrane proteins, synaptophysin and vesicle-associated memb
rane protein/synaptobrevin-2, indicating that syntaxin molecules are c
oncentrated in the presynaptic terminals. Botulinum neurotoxin C-1 app
lied extracellularly or intracellularly into presynaptic neurons block
ed synaptic transmission. Introduction of a monoclonal antibody, or po
lyclonal antibodies, to syntaxin into the presynaptic neuron depressed
the evoked release of acetylcholine without affecting Ca2+ influx thr
ough Ca2+ channels. These results suggest that syntaxin plays an impor
tant role in release of neurotransmitter by a nerve impulse and that t
his mechanism is downstream of Ca2+ influx.