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The Journal of Neuroscience, November 15, 2000, 20(22):8614-8619

Key Role for the Epsilon Isoform of Protein Kinase C in Painful Alcoholic Neuropathy in the Rat

Olayinka A. Dina¹, Justine Barletta¹, Xiaojie Chen¹, Annick Mutero¹, Annick Martin², Robert O. Messing², and Jon D. Levine¹

¹ Departments of Medicine and Oral and Maxillofacial Surgery, Division of Neuroscience and Biomedical Sciences Program, National Institutes of Health Pain Center (UCSF), University of California at San Francisco, San Francisco, California 94143-0440, and ² Department of Neurology, University of California at San Francisco and Ernest Gallo Clinic and Research Center, Emeryville, California 94608

Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliably successful therapy, attributable to, in great part, a lack of understanding of the underlying mechanisms. We tested the hypothesis that neuropathic pain associated with chronic alcohol consumption is a result of abnormal peripheral nociceptor function. In rats maintained on a diet to simulate chronic alcohol consumption in humans, mechanical hyperalgesia was present by the fourth week and maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present. Mechanical threshold of C-fibers in ethanol fed rats was lowered, and the number of action potentials during sustained stimulation increased. The hyperalgesia was acutely attenuated by intradermal injection of nonselective protein kinase C (PKC) or selective PKC inhibitors injected at the site of nociceptive testing. Western immunoblot analysis indicated a higher level of PKC in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKC second-messenger signaling in nociceptors contributing to alcohol-induced hyperalgesia.

Key words: protein kinase C ; alcoholic peripheral neuropathy; pain; hyperalgesia; allodynia; primary afferent nociceptor

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20228614-06$05.00/0

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