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Peripheral inflammation suppresses inward rectifying potassium currents of satellite glial cells in the trigeminal ganglia

Takeda, Mamorua,*; Takahashi, Masayukia; Nasu, Masanorib; Matsumoto, Shigejia

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doi: 10.1016/j.pain.2011.05.023
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Summary Inflammation suppresses satellite glial inward rectifying K+ (Kir) currents in the trigeminal ganglia. Kir channel may be a potential therapeutic target for treatment of pain.

ABSTRACT Previous studies indicate that silencing Kir4.1, a specific inward rectifying K+ (Kir) channel subunit, in sensory ganglionic satellite glial cells (SGCs) induces behavioral hyperalgesia. However, the function of Kir4.1 channels in SGCs in vivo under pathophysiological conditions remains to be determined. The aim of the present study was to examine whether peripheral inflammation in anesthetized rats alters the SGC Kir4.1 current using in vivo patch clamp and immunohistochemical techniques. Inflammation was induced by injection of complete Freund’s adjuvant into the whisker pad. The threshold of escape from mechanical stimulation applied to the orofacial area in inflamed rats was significantly lower than in naïve rats. The mean percentage of small/medium diameter trigeminal ganglion (TRG) neurons encircled by Kir4.1-immunoreactive SGCs in inflamed rats was also significantly lower than in naïve rats. In vivo whole-cell recordings were made using SGCs in the trigeminal ganglia (TRGs). Increasing extracellular K+ concentrations resulted in significantly smaller potentiation of the mean peak amplitude of the Kir current in inflamed compared with naïve rats. In addition, the density of the Ba2+-sensitive Kir current associated with small-diameter TRG neurons was significantly lower in inflamed rats compared with naïve rats. Mean membrane potential in inflamed rats was more depolarized than in naïve rats. These results suggest that inflammation could suppress Kir4.1 currents of SGCs in the TRGs and that this impairment of glial potassium homeostasis in the TRGs contributes to trigeminal pain. Therefore, the Kir4.1 channel in SGCs may be a new molecular target for the treatment of trigeminal inflammatory pain.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

aDepartment of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan

bResearch Center for Odontology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan

*Corresponding author. Tel./fax: +81 3 3261 8740.

E-mail address:m-takeda@tokyo.ndu.ac.jp

Article history: Received 3 August 2010; Received in revised form 13 May 2011; Accepted 18 May 2011.

© 2011 Lippincott Williams & Wilkins, Inc.
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