Modification of the fenvalerate-induced nociceptive response in mice by diabetes |
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Authors: | Kamei Junzo Iguchi Emiko Sasaki Mitsumasa Zushida Ko Morita Kayo Tanaka Shun-ichi |
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Affiliation: | Department of Pathophysiology and Therapeutics, Faculty of Pharmaceutical Sciences, Hoshi University, 4-41, Ebara 2-Chome, Shinagawa-ku, Tokyo 142-8501, Japan. kamei@hoshi.ac.jp |
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Abstract: | We examined the effect of diabetes on the fenvalerate-induced nociceptive response in mice. The intrathecal (i.t.) or intraplantar (i.pl.) injection of fenvalerate, a sodium channel activator, induced a characteristic behavioral syndrome mainly consisting of reciprocal hind limb scratching directed towards caudal parts of the body and biting or licking of the hind legs in both non-diabetic and diabetic mice. However, the intensity of such fenvalerate-induced nociceptive responses was significantly greater in diabetic mice than in non-diabetic mice. Calphostin C (3 pmol, i.t.), a selective protein kinase C inhibitor, significantly inhibited intrathecal fenvalerate-induced nociceptive behavior with a rightward shift of the dose-response curve for fenvalerate-induced nociceptive behavior to the level those observed in non-diabetic mice. On the other hand, when non-diabetic mice were pretreated with phorbol-12, 13-dibutyrate (50 pmol, i.t.), the dose-response curve for intrathecal fenvalerate-induced nociceptive behavior was shifted leftward to the level those observed in diabetic mice. These results suggest that the sensitization of sodium channels, probably tetrodotoxin-resistant (TTX-R) sodium channels, by the long-term activation of protein kinase C may play an important role in the enhancement of the duration of fenvalerate-induced nociceptive behavior in diabetic mice. |
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Keywords: | Diabetes Nociception Fenvalerate TTX-R sodium channel Protein kinase C |
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