Functional expression of TRPV1 and TRPA1 in rat vestibular ganglia

• Published in: Neuroscience letters 2013-09, Vol.552, p.92-97
• Main Authors: Kamakura, Takefumi, Ishida, Yusuke, Nakamura, Yukiko, Yamada, Takahiro, Kitahara, Tadashi, Takimoto, Yasumitsu, Horii, Arata, Uno, Atsuhiko, Imai, Takao, Okazaki, Suzuyo, Inohara, Hidenori, Shimada, Shoichi
• Format: Article
• Language: English
• Subjects: Acetanilides - pharmacology; Acrolein - analogs & derivatives; Acrolein - pharmacology; Animals; Ca2+ imaging experiment; Calcium - metabolism; Capsaicin - analogs & derivatives; Capsaicin - pharmacology; In situ hybridization; Molecular Imaging; Primary Cell Culture; Purines - pharmacology; Rats; TRPA1; TRPA1 Cation Channel; TRPC Cation Channels - agonists; TRPC Cation Channels - antagonists & inhibitors; TRPC Cation Channels - biosynthesis; TRPC Cation Channels - physiology; TRPV Cation Channels - agonists; TRPV Cation Channels - antagonists & inhibitors; TRPV Cation Channels - biosynthesis; TRPV Cation Channels - physiology; TRPV1; Vestibular ganglia; Vestibular Nerve - drug effects; Vestibular Nerve - metabolism
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2013.07.019

•TRPV1 and TRPA1 RT-PCR products were amplified from the mRNA of rat VG neurons.•In situ hybridization showed TRPV1 and TRPA1 mRNA expression in VG neurons.•Immunohistochemistry experiments confirmed TRPV1 protein expression.•Ca2+ imaging revealed functional TRPV1 and TRPA1 expression in VG neurons.•TRPV1 and TRPA1 might participate in vestibular function and related dysfunctions. Both TRPV1 and TRPA1 are non-selective cation channels. They are co-expressed, and interact in sensory neurons such as dorsal root ganglia (DRG) and trigeminal ganglia (TG), and are involved in nociception, being activated by nociceptive stimuli. Immunohistological localization of TRPV1 in vestibular ganglion (VG) neurons has been reported. Although TRPA1 is co-expressed with TRPV1 in DRG and TG neurons, it is unclear whether TRPA1 channels are expressed in VG neurons. Moreover, it is unknown whether TRPV1 and TRPA1 channels are functional in VG neurons. We investigated the expression of TRPV1 and TRPA1 in rat VG neurons by RT-PCR, in situ hybridization, immunohistochemistry, and Ca2+ imaging experiments. Both TRPV1 and TRPA1 RT-PCR products were amplified from the mRNA of rat VG neurons. In situ hybridization experiments showed TRPV1 and TRPA1 mRNA expression in the majority of VG neurons. Immunohistochemistry experiments confirmed TRPV1 protein expression. In Ca2+ imaging experiments, capsaicin, a TRPV1 agonist, induced a significant increase in intracellular calcium ion concentration ([Ca2+]i) in rat primary cultured VG neurons, which was almost completely blocked by capsazepine, a TRPV1-specific antagonist. Cinnamaldehyde, a TRPA1 agonist, also caused an increase in [Ca2+]i, which was completely inhibited by HC030031, a TRPA1-specific antagonist. Moreover, in some VG neurons, a [Ca2+]i increase was evoked by both capsaicin and cinnamaldehyde in the same neuron. In summary, our histological and physiological studies reveal that TRPV1 and TRPA1 are expressed in VG neurons. It is suggested that TRPV1 and TRPA1 in VG neurons might participate in vestibular function and/or dysfunction such as vertigo.