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Journal of Neuroscience, Vol 12, 3671-3675, Copyright © 1992 by Society for Neuroscience
The role of NMDA receptor-operated calcium channels in persistent nociception after formalin-induced tissue injury
TJ Coderre and R Melzack
Pain Mechanisms Laboratory, Clinical Research Institute of Montreal, Quebec, Canada.
The contribution of intracellular calcium to central sensitization and
persistent nociception in response to tissue injury in rats was examined
following the subcutaneous injection of formalin into the hindpaw. Formalin
injury-induced nociceptive behaviors were enhanced by intrathecal
pretreatment with the calcium ionophore A23187 or the calcium channel
agonist Bay-K8644. Conversely, formalin nociceptive responses were reduced
by intrathecal pretreatment with the calcium chelator Quin 2 or the calcium
channel antagonists verapamil and nifedipine. Each of these agents affected
the tonic, but not the acute, phase of the formalin response. The
enhancement in formalin nociceptive behavior in rats treated with
L-aspartate or L-glutamate was reversed by combined pretreatment with the
noncompetitive NMDA antagonist MK- 801, but not by nifedipine or the
non-NMDA excitatory amino acid antagonist
6-cyano-7-dinitroquinoxaline-2,3-dione. In rats not treated with excitatory
amino acids, the analgesic effect of MK-801 was also significantly greater
than that produced by nifedipine. Furthermore, combining nifedipine with
MK-801 did not produce a significantly greater analgesic effect than MK-801
alone. The results suggest that central sensitization and persistent
nociception following formalin- induced tissue injury are dependent on the
influx of calcium through predominantly NMDA receptor-operated (and to a
lesser extent voltage- gated) calcium channels.
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