Vesicle hypothesis of the release of quanta of acetylcholine.

Calcium currents at motor nerve endings: absence of effects of adenosine receptor agonists in the frog.

“…While Ca2+ currents evoked by K+ depolarization cannot be measured in frog motor nerve endings, an indirect means of studying the effect of adenosine on Ca2+ movements is provided by reversing the electrochemical gradient for Ca2+ from inward to outward. In contrast to the stimulatory effects of K+ depolarization on MEPP frequency in normal Ca2+ solutions (Ceccarelli & Hurlbut, 1980;Silinsky, 1988), K+ depolarization in a reverse Ca2+ gradient reduces MEPP frequency (Rotshenker, Erulkar & Rahamimoff, 1976;Shimoni et al 1977;Zucker & Lando, 1986). This depression in MEPP frequency is explained by the departure of Ca2+ from the nerve ending down its concentration gradient, reducing its availability to promote the secretary process (e.g.…”

Temporal coincidence between synaptic vesicle fusion and quantal secretion of acetylcholine.

“…Quantal secretion causes the changes in membrane potential that excite the postsynaptic cell, and transmission at a synapse is critically dependent upon this mechanism of release. The vesicle hypothesis holds that each quantum is confined within one of the synaptic vesicles that populate the nerve terminal and is released by exocytosis when the membrane of that vesicle fuses with the axolemma at one of the many specialized regions called "active zones" (8,13,51).A number of workers have shown that at frog neuromuscular junctions vesicles fuse with the axolemma of stimulated 1386 terminals and some of the remaining vesicles become labeled with extracellular tracers (9)(10)(11)25). Although these observations indicate that vesicles fuse with and are recovered from the axolemma when quanta are actively secreted, the slowness of chemical fixation precludes demonstrating that vesicle fusion and transmitter release are coincident.…”

“…Quantal secretion causes the changes in membrane potential that excite the postsynaptic cell, and transmission at a synapse is critically dependent upon this mechanism of release. The vesicle hypothesis holds that each quantum is confined within one of the synaptic vesicles that populate the nerve terminal and is released by exocytosis when the membrane of that vesicle fuses with the axolemma at one of the many specialized regions called "active zones" (8,13,51).…”

“…First, it would allow quanta of transmitter to escape while rapidly recovering vesicles for subsequent release, with minimal intermixing of membrane components (36). Second, it would save the work required to invaginate the flattened patches of membrane (8).…”

Developmental Biology of Neoplastic Growth

“…1b) (Kreger et al 1993) leading to a specific depletion of small clear synaptic vesicles and subsequent neuromuscular paralysis (Colasante et al 1996). This effect is reminiscent of the stimulatory effect observed on the same preparation when treated with α-latrotoxin from the venom of the black widow spider Latrodectus mactans tredecimguttatus (see review by Ceccarelli and Hurlbut 1980). The similarity in effect between the two neurotoxins is even greater as both seem to selectively act on small synaptic vesicles without affecting the release of large dense core vesicles at the frog presynaptic motor nerve terminals (Fig.…”