Glutamate-induced calcium transients in rat neurons of the dorsal motor nucleus of the vagus.

The dorsal motor nucleus of the vagus (DMNV) integrates peripheral and central signals and sends efferent output to the gastrointestinal system. Glutamate, the major excitatory neurotransmitter of the central nervous system, causes increases in intracellular calcium in DMNV neurons. The mechanisms by which glutamate activates calcium signaling in the DMNV were examined. DMNV neurons were isolated from neonatal rat brainstem using microdissection and enzymatic digestion. Exposure to glutamate caused intracellular Ca(2+) increments in greater than 80% of cells. Removal of extracellular Ca(2+) abolished intracellular Ca(2+) transients. Kynurenic acid, a nonspecific glutamate receptor antagonist, abolished intracellular Ca(2+) transients. Exposure to glutamate while blocking AMPA receptors with GYKI 52466 abolished the Ca(2+) response. Exposure to (S)AMPA, an AMPA receptor agonist, caused intracellular Ca(2+) increments in 97% of cells. Activation and antagonism of NMDA and kainate receptors produced no changes compared to control experiments. NiCl, a nonspecific Ca(2+) channel blocker, abolished intracellular Ca(2+) transients. Blocking T-type Ca(2+) channels with mibefradil abolished the Ca(2+) response in 76% of cells. Blockade of L-type and N-type Ca(2+) channels did not affect the Ca(2+) response. Glutamate mediates intracellular Ca(2+) currents in DMNV neurons via the AMPA receptor and T-type Ca(2+) channels, allowing influx of extracellular Ca(2+).