Possible roles of synaptic vesicles in plasticity of enhanced neurotransmission via Ca²⁺-induced Ca²⁺ release at frog motor nerve terminal.

Abstract

Ca²⁺-induced Ca²⁺ release (CICR) takes place in response to Ca²⁺ entry via the activation of type-3 ryanodine receptors (RyRs) after its use- and Ca²⁺-dependent priming, and amplifies impulse-evoked transmitter release in frog motor nerve terminals. Since the activation of CICR occurs in less than 1 msec after a nerve impulse, the site of Ca²⁺ release is close to the high [Ca²⁺]_i microdomain, where the machinery of the exocytosis is activated. Then, the most possible Ca²⁺ stores, on which RyRs reside, would be synaptic vesicles. We studied here the effects of loading Ca²⁺ chelator into synaptic vesicles on the priming and induction of CICR. EGTA was loaded into synaptic vesicles by incubating preparations in a Ca²⁺-free, EGTA (1mM) and Mg²⁺ (1 or 10mM) solution for 20-30 min, in which endocytosis still took place following high frequency stimulation of the nerve in low Ca²⁺ (0.15-0.5mM), high Mg²⁺ (6-10mM) solutions. After loading EGTA, tetanus-induced rises in end-plate potential (EPP) amplitude and miniature EPP (MEPP) frequency, reflecting the priming and activattion of CICR, became slower in onset and smaller in amplitude and rate of rise. Results are in favor of the idea that synaptic vesicles are involved in the priming and activation of CICR and so synaptic plasticity. [J Physiol Sci. 2006;56 Suppl:S167]