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Ca(2+)-dependent neurotransmitter release was originally thought to occur only following activation of presynaptic voltage-gated calcium channels after a presynaptic action potential. Recent evidence suggests that not only opening of voltage-gated but also ligand-gated ion channels, such as neurotransmitter receptors, can trigger exocytosis, as well as Ca(2+) release from intracellular Ca(2+) stores. It was shown that activation of N-methyl-d-aspartate (NMDA) receptors on presynaptic interneurons led to increases in GABA release from these neurons onto postsynaptic Purkinje cells in rat cerebellum in the presence of tetrodotoxin (TTX), suggesting a presynaptic location for the underlying NMDA receptors. However, the mechanism for the NMDA-induced increase in GABA release remained unclear. The present study addresses the question whether Ca(2+) influx through presynaptic NMDA receptors alone is sufficient to trigger presynaptic GABA release at this synapse or whether activation of presynaptic NMDA receptors leads to opening of voltage-gated Ca(2+) channels, thereby increasing exocytosis. The results suggest that the NMDA-induced increase in presynaptic GABA release neither requires activation of presynaptic voltage-gated Ca(2+) channels nor Ca(2+) release from presynaptic Ca(2+) stores. It is concluded that Ca(2+) influx through the NMDA receptor alone is sufficient to drive presynaptic GABA release at the rat interneuron-Purkinje cell synapse.

Original publication

DOI

10.1016/j.neuroscience.2007.10.024

Type

Journal article

Journal

Neuroscience

Publication Date

24/01/2008

Volume

151

Pages

403 - 409

Keywords

Animals, Cadmium, Calcium, Calcium Channel Blockers, Calcium Channels, Calcium Signaling, Cerebellum, Electrophysiology, Excitatory Amino Acid Agonists, Interneurons, N-Methylaspartate, Patch-Clamp Techniques, Purkinje Cells, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate, Receptors, Presynaptic, Synapses, gamma-Aminobutyric Acid