TY - JOUR
T1 - Capsaicin-Sensitive Sensory Nerves Mediate the Cellular and Microvascular Effects of H2S via TRPA1 Receptor Activation and Neuropeptide Release
AU - Hajna, Zsófia
AU - Sághy, Éva
AU - Payrits, Maja
AU - Aubdool, Aisah
AU - Szőke, Éva
AU - Pozsgai, Gábor
AU - Bátai, István Z.
AU - Nagy, Lívia
AU - Filotás, Dániel
AU - Helyes, Zsuzsanna
AU - Brain, Susan D.
AU - Pintér, Erika
PY - 2016/8/15
Y1 - 2016/8/15
N2 - It is supposed that TRPA1 receptor can be activated by hydrogen sulphide (H2S). Here, we have investigated the role of TRPA1 receptor in H2S-induced [Ca2+]i increase in trigeminal ganglia (TRG) neurons, and the involvement of capsaicin-sensitive sensory nerves in H2S-evoked cutaneous vasodilatation. [Ca2+]i was measured with ratiometric technique on TRG neurons of TRPA1+/+ and TRPA1−/− mice after NaHS, Na2S, allylisothiocyanate (AITC) or KCl treatment. Microcirculatory changes in the ear were detected by laser Doppler imaging in response to topical NaHS, AITC, NaOH, NaSO3 or NaCl. Mice were either treated with resiniferatoxin (RTX), or CGRP antagonist BIBN4096, or NK1 receptor antagonist CP99994, or K+ ATP channel blocker glibenclamide. Alpha-CGRP−/− and NK1 −/− mice were also investigated. NaHS and Na2S increased [Ca2+]i in TRG neurons derived from TRPA+/+ but not from TRPA1−/− mice. NaHS increased cutaneous blood flow, while NaOH, NaSO3 and NaCl did not cause significant changes. NaHS-induced vasodilatation was reduced in RTX-treated animals, as well as by pre-treatment with BIBN4096 or CP99994 alone or in combination. NaHS-induced vasodilatation was significantly smaller in alpha-CGRP−/− or NK1 −/− mice compared to wild-types. H2S activates capsaicin-sensitive sensory nerves through TRPA1 receptors and the resultant vasodilatation is mediated by the release of vasoactive sensory neuropeptides CGRP and substance P.
AB - It is supposed that TRPA1 receptor can be activated by hydrogen sulphide (H2S). Here, we have investigated the role of TRPA1 receptor in H2S-induced [Ca2+]i increase in trigeminal ganglia (TRG) neurons, and the involvement of capsaicin-sensitive sensory nerves in H2S-evoked cutaneous vasodilatation. [Ca2+]i was measured with ratiometric technique on TRG neurons of TRPA1+/+ and TRPA1−/− mice after NaHS, Na2S, allylisothiocyanate (AITC) or KCl treatment. Microcirculatory changes in the ear were detected by laser Doppler imaging in response to topical NaHS, AITC, NaOH, NaSO3 or NaCl. Mice were either treated with resiniferatoxin (RTX), or CGRP antagonist BIBN4096, or NK1 receptor antagonist CP99994, or K+ ATP channel blocker glibenclamide. Alpha-CGRP−/− and NK1 −/− mice were also investigated. NaHS and Na2S increased [Ca2+]i in TRG neurons derived from TRPA+/+ but not from TRPA1−/− mice. NaHS increased cutaneous blood flow, while NaOH, NaSO3 and NaCl did not cause significant changes. NaHS-induced vasodilatation was reduced in RTX-treated animals, as well as by pre-treatment with BIBN4096 or CP99994 alone or in combination. NaHS-induced vasodilatation was significantly smaller in alpha-CGRP−/− or NK1 −/− mice compared to wild-types. H2S activates capsaicin-sensitive sensory nerves through TRPA1 receptors and the resultant vasodilatation is mediated by the release of vasoactive sensory neuropeptides CGRP and substance P.
KW - Capsaicin-sensitive sensory neuron
KW - CGRP
KW - Hydrogen sulphide
KW - Substance P
KW - TRPA1 receptor
UR - http://www.scopus.com/inward/record.url?scp=84982082481&partnerID=8YFLogxK
U2 - 10.1007/s12031-016-0802-z
DO - 10.1007/s12031-016-0802-z
M3 - Article
AN - SCOPUS:84982082481
SN - 0895-8696
SP - 1
EP - 14
JO - Journal of molecular neuroscience
JF - Journal of molecular neuroscience
ER -