Title: | "Multiple cation channels mediate increases in intracellular calcium induced by the volatile irritant, trans-2-pentenal in rat trigeminal neurons" |
Address: | "Tobacco Science Research Center, Japan Tobacco Inc., Yokohama, Kanagawa, 227-8512, Japan. takashi.c.inoue@jt.com" |
DOI: | 10.1007/s10571-009-9428-9 |
ISSN/ISBN: | 1573-6830 (Electronic) 0272-4340 (Linking) |
Abstract: | "Trans-2-Pentenal (pentenal), an alpha,beta-unsaturated aldehyde, induces increases in [Ca(2+)](i) in cultured neonatal rat trigeminal ganglion (TG) neurons. Since all pentenal-sensitive neurons responded to a specific TRPA1 agonist, allyl isothiocyanate (AITC) and neurons from TRPA1 knockouts failed to respond to pentenal, TRPA1 appears to be sole initial transduction site for pentenal-evoked trigeminal response, as reported for the structurally related irritant, acrolein. Furthermore, because the neuronal sensitivity to pentenal is strictly dependent upon the presence of extracellular Na(+)/Ca(2+), as we showed previously, we investigated which types of voltage-gated sodium/calcium channels (VGSCs/VGCCs) are involved in pentenal-induced [Ca(2+)](i) increases as a downstream mechanisms. The application of tetrodotoxin (TTX) significantly suppressed the pentenal-induced increase in [Ca(2+)](i) in a portion of TG neurons, suggesting that TTX-sensitive (TTXs) VGSCs contribute to the pentenal response in those neurons. Diltiazem and omega-agatoxin IVA, antagonists of L- and P/Q-type VGCCs, respectively, both caused significant reductions of the pentenal-induced responses. omega-Conotoxin GVIA, on the other hand, caused only a small decrease in the size of pentenal-induced [Ca(2+)](i) rise. These indicate that both L- and P/Q-type VGCCs are involved in the increase in [Ca(2+)](i) produced by pentenal, while N-type calcium channels play only a minor role. This study demonstrates that TTXs VGSCs, L- and P/Q-type VGCCs play a significant role in the pentenal-induced trigeminal neuronal responses as downstream mechanisms following TRPA1 activation" |
Keywords: | Aldehydes/*pharmacology Animals Calcium/*metabolism Calcium Channel Blockers/pharmacology Calcium Channels/metabolism Calcium Signaling/drug effects Extracellular Space/metabolism Intracellular Space/drug effects/*metabolism Ion Channel Gating/drug effect; |
Notes: | "MedlineInoue, Takashi Bryant, Bruce P eng Research Support, Non-U.S. Gov't 2009/07/02 Cell Mol Neurobiol. 2010 Jan; 30(1):35-41. doi: 10.1007/s10571-009-9428-9. Epub 2009 Jun 30" |