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Brain research bulletin · Jul 2014
Expression of transient receptor potential vanilloid 1 and anoctamin 1 in rat trigeminal ganglion neurons innervating the tongue.
- Takuya Kanazawa and Shigeji Matsumoto.
- Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan. Electronic address: kanazawa@tky.ndu.ac.jp.
- Brain Res. Bull. 2014 Jul 1;106:17-20.
AbstractTransient receptor potential vanilloid 1 (TRPV1) is a polymodal sensor that is activated by heat (>43 °C), acid, or capsaicin, the pungent ingredient of hot peppers. Reports that mice lacking TRPV1 display heat avoidance behaviors and TRPV1-negative neurons respond to heat suggest that an additional heat sensor is present. Anoctamin 1 (ANO1; also known as transmembrane protein 16A [TMEM16A]), is a component of Ca(2+)-activated chloride channels (CaCCs), and has been recently identified as a heat sensor, activated by temperatures over 44 °C. ANO1 is highly co-localized with TRPV1 in small-diameter dorsal root ganglion (DRG) neurons. The aim of the present study was to investigate co-expression of ANO1 and TRPV1 in rat trigeminal ganglion (TG) neurons innervating the tongue by using retrograde labeling and immunohistochemical techniques. Fluoro-gold (FG) retrograde labeling was used to identify the TG neurons innervating the anterior two thirds of the tongue; as expected, most labeling was detected in the mandibular division of the TGs. The FG-labeled TG neurons showed TRPV1 immunoreactivity (17.9%) and ANO1 immunoreactivity (13.7%), indicating that TRPV1- and ANO1-expressing neurons were present in the mandibular division of the TGs. Seventy-six percent of the ANO1-immunoreactive TG neurons were also immunoreactive for TRPV1; this co-expression was mainly detected in small- to medium-diameter TG neurons. The high degree of co-expression of TRPV1 and ANO1 suggests that cooperation between ANO1 and TRPV1 plays a role in the signaling pathways of nociceptive TG neurons.Copyright © 2014 Elsevier Inc. All rights reserved.
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