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Fig. 8. Potential role for RyR and snapin in neurotransmitter release. (A) The arrival of an action potential at the presynaptic terminal causes plasma membrane depolarisation and Ca²⁺ entry through voltage-operated Ca²⁺ channels. Ca²⁺ entry induces fusion of synaptic vesicles (SV) with the plasma membrane through a process involving the SNARE core complex and synaptotagmin, and this process is reinforced through the interaction of snapin with SNAP25. In addition, Ca²⁺ entry activates RyR channels that are mobilising Ca²⁺ from internal stores. RyR channel activation and/or the rise in intracellular Ca²⁺ might cause snapin dissociation from the RyR and translocation to SNAP25, resulting in further enhancement of neurotransmitter release. (B) Ca²⁺ entry through voltage-operated Ca²⁺ channels induces fusion of synaptic vesicles with the plasma membrane and consequent neurotransmitter release. Furthermore, RyR channels located on the endoplasmic reticulum (ER) are activated by the Ca²⁺-induced Ca²⁺-release mechanism and provide an additional source of Ca²⁺. Snapin interaction with the RyR might increase channel open probability and result in augmented Ca²⁺ release. (C) In the absence of plasma membrane depolarisation, some membrane fusion events still occur, most probably as a result of spontaneous localised Ca²⁺-release events from ryanodine-sensitive Ca²⁺ stores. Snapin interaction with the RyR might increase Ca²⁺ spark frequency and/or amplitude, accounting for spontaneous neurotransmitter release.

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