Genetic deletion of Cav3.2 T-type calcium channels abolishes H2S-dependent somatic and visceral pain signaling in C57BL/6 mice.
J Pharmacol Sci
; 140(3): 310-312, 2019 Jul.
Article
in En
| MEDLINE
| ID: mdl-31492577
ABSTRACT
We tested whether genetic deletion of Cav3.2 T-type Ca2+ channels abolishes hydrogen sulfide (H2S)-mediated pain signals in mice. In Cav3.2-expressing HEK293 cells, Na2S, an H2S donor, at 100 µM clearly increased Ba2+ currents, as assessed by whole-cell patch-clamp recordings. In wild-type C57BL/6 mice, intraplantar and intracolonic administration of Na2S evoked mechanical allodynia and visceral nociceptive behavior, respectively, which were abolished by TTA-A2, a T-type Ca2+ channel blocker. In Cav3.2-knockout mice of a C57BL/6 background, Na2S caused neither somatic allodynia nor colonic nociception. Our study thus provides definitive evidence for an essential role of Cav3.2 in H2S-dependent somatic and colonic pain.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Signal Transduction
/
Calcium Channels, T-Type
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Nociceptive Pain
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Visceral Pain
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Hydrogen Sulfide
Limits:
Animals
/
Humans
Language:
En
Year:
2019
Type:
Article