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Vol. 282, Issue 3, 1319-1325, 1997
Department of Veterinary PathoBiology, University of Minnesota, St.
Paul, Minnesota
Zinc is concentrated in the dorsal horn of the spinal cord and has been
proposed to alter excitability of primary afferent C-fibers, structures
believed to be important in nociceptive transmission. Based on the
inhibitory effect of zinc on the activity of various other
neurotransmitters that play a role in nociception, we tested the
hypothesis that zinc modulates pain transmission. To test this, we
examined the effect of exogenous zinc, administered intrathecally (i.t.), on nociception in the mouse. We also assessed the impact of
decreased concentrations of endogenously occurring zinc in the
extracellular fluid brought about by an i.t. injection of either
ethylenediaminetetraacetic acid disodium-calcium salt
(Ca++EDTA), a calcium-saturated, membrane-impermeable
chelator of divalent cations, or of dipicolinic acid, a zinc chelator.
Injection of zinc produced a dose-related antinociceptive effect,
optimal at 90 min in the writhing assay, but had no effect on
tail-flick response latencies. In contrast, injection of either
Ca++EDTA or dipicolinic acid produced a dose-related
hyperalgesia in the tail-flick assay at 90 min after injection.
Responses induced in the writhing assay were unaffected by
Ca++EDTA. Although zinc had no effect on thermal
nociception, the hyperalgesic effect of Ca++EDTA was
antagonized by coadministration of Ca++EDTA with zinc.
Similarly, the antinociceptive effect of zinc on writhing responses was
attenuated when coadministered with Ca++EDTA. Zinc also
inhibited primary afferent C-fiber activity because 10 ng of zinc i.t.
inhibited the behavioral response induced by injection i.t. of 1 nmol
of capsaicin. Neither zinc nor Ca++EDTA altered writhing or
tail-flick latencies, respectively, when injected
intracerebroventricularly. These findings support the hypothesis that
endogenous zinc, localized in the dorsal horn of the spinal cord, plays
a role in the regulation of pain.
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