AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 6 1423-R1428, Copyright © 1995 by American Physiological Society
Sensitization of nociceptive C-fibers in zinc-deficient rats
H. Izumi, H. Mori, T. Uchiyama, S. Kuwazuru, Y. Ozima, I. Nakamura and S. Taguchi
Department of Physiology, Tohoku University School of Dentistry, Sendai, Japan.
A marked decrease in zinc concentration was observed in plasma (P <
0.001), hindpaw skin (P < 0.01), and dorsal skin (P < 0.01) in
zinc-deficient rats (rats fed a zinc-deficient diet for 3 wk), compared
with the control rats fed the same zinc-deficient diet supplemented with
ZnCO3 (50 mg/kg diet). The threshold intensity needed to elicit
vasodilatation in the hindpaw skin of the zinc-deficient rats on electrical
stimulation of the saphenous nerve in a peripheral direction was markedly
lower (P < 0.01) than that in the control rats. No difference was
observed between control (n = 5) and zinc-deficient rats (n = 5) in the
magnitude of the plasma extravasation evoked by either histamine or
substance P. There was no difference between control and zinc-deficient
rats in terms of the dose-response curve for release of histamine by
substance P. Prostaglandin E2 (PGE2) concentration in the hindpaw skin of
the zinc-deficient rats was nearly fourfold higher (P < 0.01) than that
of the control rats, whereas no difference in the leukotriene B4 level in
the hindpaw skin was observed between control and zinc-deficient rats. From
the present study, it seems likely that an increased level of PGE2 in the
vicinity of the nociceptive C-fiber terminals in the hindpaw skin of
zinc-deficient rats may sensitize the terminals of the nociceptive C-fibers
of the saphenous afferent nerve in the hindpaw and thus facilitate the
production of antidromic vasodilatation.
