Calcium transients and neurotransmitter release at an identified synapse

It is widely accepted that the modulation of the presynaptic Ca2+ influx is one of the main mechanisms by which neurotransmitter release can be contro lled. The well-identified cholinergic synapse in the buccal ganglion of Apl ysia has been used to study the modulations that affect presynaptic Ca2+ tr ansients and to relate this to quantal evoked neurotransmitter release. Thr ee types of Ca2+ channel (L, N and P) are present in the presynaptic neuron e at this synapse. Influxes of Ca2+ through N- and P-type channels trigger the release of ACh with only N-type Ca2+ channels being regulated by presyn aptic neuromodulator receptors. In addition, presynaptic Ca2+ stores, via c omplex mechanisms of Ca2+ uptake and Ca2+ release, control the Ca2+ concent ration that triggers this evoked ACh release.