{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,5]],"date-time":"2025-11-05T10:54:17Z","timestamp":1762340057282,"version":"3.41.2"},"reference-count":29,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2006,1,1]],"date-time":"2006-01-01T00:00:00Z","timestamp":1136073600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mol Pain"],"published-print":{"date-parts":[[2006,1,1]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p> Triptans, 5-HT<jats:sub>1B\/ID<\/jats:sub> agonists, act on peripheral and\/or central terminals of trigeminal ganglion neurons (TGNs) and inhibit the release of neurotransmitters to second-order neurons, which is considered as one of key mechanisms for pain relief by triptans as antimigraine drugs. Although high-voltage activated (HVA) Ca<jats:sup>2+<\/jats:sup> channels contribute to the release of neurotransmitters from TGNs, electrical actions of triptans on the HVA Ca<jats:sup>2+<\/jats:sup> channels are not yet documented. <\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p> In the present study, actions of zolmitriptan, one of triptans, were examined on the HVA Ca<jats:sup>2+<\/jats:sup> channels in acutely dissociated rat TGNs, by using whole-cell patch recording of Ba<jats:sup>2+<\/jats:sup> currents (I<jats:sub>Ba<\/jats:sub>) passing through Ca<jats:sup>2+<\/jats:sup> channels. Zolmitriptan (0.1\u2013100 \u03bcM) reduced the size of I<jats:sub>Ba<\/jats:sub> in a concentration-dependent manner. This zolmitriptan-induced inhibitory action was blocked by GR127935, a 5-HT<jats:sub>1B\/1D<\/jats:sub> antagonist, and by overnight pretreatment with pertussis toxin (PTX). P\/Q-type Ca<jats:sup>2+<\/jats:sup> channel blockers inhibited the inhibitory action of zolmitriptan on I<jats:sub>Ba<\/jats:sub>, compared to N-and L-type blockers, and R-type blocker did, compared to L-type blocker, respectively (p &lt; 0.05). All of the present results indicated that zolmitriptan inhibited HVA P\/Q- and possibly R-type channels by activating the 5-HT<jats:sub>1B\/1D<\/jats:sub> receptor linked to G<jats:sub>i\/o<\/jats:sub> pathway. <\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p> It is concluded that this zolmitriptan inhibition of HVA Ca<jats:sup>2+<\/jats:sup> channels may explain the reduction in the release of neurotransmitters including CGRP, possibly leading to antimigraine effects of zolmitriptan. <\/jats:p><\/jats:sec>","DOI":"10.1186\/1744-8069-2-10","type":"journal-article","created":{"date-parts":[[2006,4,6]],"date-time":"2006-04-06T13:30:18Z","timestamp":1144330218000},"source":"Crossref","is-referenced-by-count":10,"title":["Antimigraine Drug, Zolmitriptan, Inhibits High-Voltage Activated Calcium Currents in a Population of Acutely Dissociated Rat Trigeminal Sensory Neurons"],"prefix":"10.1177","volume":"2","author":[{"given":"Tomoko","family":"Morikawa","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan"},{"name":"Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshiyasu","family":"Matsuzawa","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan"},{"name":"Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Koshi","family":"Makita","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshifumi","family":"Katayama","sequence":"additional","affiliation":[{"name":"Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, 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