Multiple Cation Channels Mediate Increases in Intracellular Calcium Induced by the Volatile Irritant, Trans-2-Pentenal in Rat Trigeminal Neurons |
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Authors: | Takashi Inoue Bruce P. Bryant |
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Affiliation: | 1. Tobacco Science Research Center, Japan Tobacco Inc., 6-2 Umegaoka, Aoba-ku, Yokohama, Kanagawa, 227-8512, Japan 2. Monell Chemical Senses Center, 3500 Market St., Philadelphia, PA, 19104, USA
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Abstract: | Trans-2-Pentenal (pentenal), an α,β-unsaturated aldehyde, induces increases in [Ca2+]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+/Ca2+, as we showed previously, we investigated which types of voltage-gated sodium/calcium channels (VGSCs/VGCCs) are involved in pentenal-induced [Ca2+]i increases as a downstream mechanisms. The application of tetrodotoxin (TTX) significantly suppressed the pentenal-induced increase in [Ca2+]i in a portion of TG neurons, suggesting that TTX-sensitive (TTXs) VGSCs contribute to the pentenal response in those neurons. Diltiazem and ω-agatoxin IVA, antagonists of L- and P/Q-type VGCCs, respectively, both caused significant reductions of the pentenal-induced responses. ω-Conotoxin GVIA, on the other hand, caused only a small decrease in the size of pentenal-induced [Ca2+]i rise. These indicate that both L- and P/Q-type VGCCs are involved in the increase in [Ca2+]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. |
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