Answers are grounded in this paper and cite their sources.
Intracellular and focal extracellular recording techniques were used to study neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals in the guinea-pig isolated vas deferens. 2. High concentrations of the selective N-type calcium channel blocker omega-conotoxin GVIA abolished the release of the neurotransmitter ATP evoked by trains of low-frequency stimuli. However, in the presence of high concentrations of the blocker, a 'residual release' persisted at higher frequencies. 3. Residual release was dependent on calcium entry through a pharmacologically distinct voltage-dependent calcium channel. 4. Residual release was inhibited by ryanodine in a use- and time-dependent manner and this inhibitory effect was potentiated by caffeine. The inhibitory effect of ryanodine on residual release was reversed by 4-aminopyridine. 5. These findings indicate that calcium-induced calcium released from intraneuronal stores plays an important role in action potential-evoked neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals.
No takes yet. Share an insight, caveat, or question.
Smith et al. (1996) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: