in the absence and presence of 50 mM KCl and/or drugs. Drugs were present as indicated during "Pretreat" and "50 mM KCl" incubations but not during the "Basal" incubation. Data is presented as the mean ± S.E.M. and the number of wells tested is indicated in parentheses. An asterisk indicates a significant difference (p < 0.05) between the transmitter release from control cells and from cells treated with calcium channel blockers. Potassium-stimulated release of glutamate was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal glutamate release was not altered (Panel A). Potassium-stimulated release of CGRP was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal CGRP release was not altered (Panel B).<p><b>Copyright information:</b></p><p>Taken from "Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling"</p><p>http://www.molecularpain.com/content/4/1/12</p><p>Molecular Pain 2008;4():12-12.</p><p>Published online 16 Apr 2008</p><p>PMCID:PMC2359740.</p><p></p
