Journal
JOURNAL OF CELL BIOLOGY
Volume 163, Issue 3, Pages 511-523Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200307027
Keywords
synaptic plasticity; neuromuscular junction; mitochondria; Na+-Ca2+ exchanger; Ca2+ influx
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Activity-dependent modulation of synaptic transmission is an essential mechanism underlying many brain functions. Here we report an unusual form of synaptic modulation that depends on Na+ influx and mitochondrial Na+-Ca2+ exchanger, but not on Ca2+ influx. in Ca2+-free medium, tetanic stimulation of Xenopus motoneurons induced a striking potentiation of transmitter release at neuromuscular synapses. Inhibition of either Na+ influx or the rise of Ca2+ concentrations ([Ca2+](i)) at nerve terminals prevented the tetanus-induced synaptic potentiation (TISP). Blockade of Ca2+ release from mitochondrial Na+-Ca2+ exchanger, but not from ER Ca2+ stores, also inhibited TISP. Tetanic stimulation in Ca2+-free medium elicited an increase in [Ca2+](i), which was prevented by inhibition of Na+ influx or mitochondrial Ca2+ release. Inhibition of PKC blocked the TISP as well as mitochondrial Ca2+ release. These results reveal a novel form of synaptic plasticity and suggest a role of PKC in mitochondrial Ca2+ release during synaptic transmission.
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