Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-3

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

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-1

Ions 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 serotonin and/or pertussis toxin. Serotonin (10 μM) inhibits KCl-stimulated but not basal release of glutamate (Panel A). Overnight pertussis toxin treatment (100 ng/ml) blocks the serotonergic inhibition of KCl-stimulated glutamate release without affecting basal or KCl-stimulated release. Serotonin (10 μM) inhibits KCl-stimulated but not basal release of CGRP (Panel B). Overnight pertussis toxin treatment (100 ng/ml) blocks the serotonergic inhibition of KCl-stimulated CGRP release without affecting basal or KCl-stimulated release from trigeminal neurons. Serotonin inhibits KCl-stimulated release of CGRP from trigeminal neurons from female rats in the absence and presence of the calcium channel blockers, 1 μM ω-Cgtx GVIA and 1 μM nimodine to a similar extent (Panel C). Serotonin (1 μM) reversibly inhibits calcium current amplitude (Panel D). Peak currents were plotted against time for this cell. The trigeminal neurons were depolarized to 0 mV for 100 msec every 20 seconds from a holding potential of -80 mV. The horizontal bar indicates perfusion of 1 μM 5-HT. Inset, superimposed current traces from the indicated time points.<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

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-0

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