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Genetic deletion of Ca3.2 T-type calcium channels abolishes HS-dependent somatic and visceral pain signaling in C57BL/6 mice.

著者 Matsui K , Tsubota M , Fukushi S , Koike N , Masuda H , Kasanami Y , Miyazaki T , Sekiguchi F , Ohkubo T , Yoshida S , Mukai Y , Oita A , Takada M , Kawabata A
J Pharmacol Sci.2019 Jul 30 ; ():.
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We tested whether genetic deletion of Ca3.2 T-type Ca channels abolishes hydrogen sulfide (HS)-mediated pain signals in mice. In Ca3.2-expressing HEK293 cells, NaS, an HS donor, at 100 μM clearly increased Ba currents, as assessed by whole-cell patch-clamp recordings. In wild-type C57BL/6 mice, intraplantar and intracolonic administration of NaS evoked mechanical allodynia and visceral nociceptive behavior, respectively, which were abolished by TTA-A2, a T-type Ca channel blocker. In Ca3.2-knockout mice of a C57BL/6 background, NaS caused neither somatic allodynia nor colonic nociception. Our study thus provides definitive evidence for an essential role of Ca3.2 in HS-dependent somatic and colonic pain.
PMID: 31492577 [PubMed - as supplied by publisher]
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