Effects of Mitochondrial Calcium Regulation on Post-tetanic Potentiation at the Crayfish Neuromuscular Junction

Abstract

Synaptic plasticity is a fundamental property of the vertebrate central nervous system and is thought to be involved in learning and memory processes. In the presynaptic terminal, mitochondria regulate synaptic plasticity by influencing neurotransmitter release. To elucidate the effect of mitochondrial calcium release on synaptic transmission and post-tetanic potentiation (PTP), a form of synaptic plasticity that has been observed at both excitatory and inhibitory synapses, we adopted the crayfish neuromuscular junction (NMJ) preparation as our model system. We employed a specific pharmacological inhibitor for mitochondria and monitored neurotransmitter release by postsynaptic electrophysiological recording. Our results demonstrated that PTP was reduced when mitochondrial Ca²⁺ release was inhibited, which suggested that PTP would be a result of the slow Ca²⁺ release from mitochondria, and that Ca²⁺ alone was able to cause substantial changes in postsynaptic PTP.