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Journal of Neuroscience, Vol 15, 8199-8213, Copyright © 1995 by Society for Neuroscience
The central nucleus of the amygdala contributes to the production of morphine antinociception in the rat tail-flick test
BH Manning and DJ Mayer
Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA.
Current models of endogenous pain control circuitry emphasize neural
substrates within the brainstem and spinal cord. We have recently shown,
however, that the central nucleus of the amygdala (Ce) contributes to
morphine-induced suppression of formalin-induced nociceptive behaviors. In
the four experiments reported here, we investigated the possibility that
the Ce also contributes to morphine- induced suppression of simple,
spinally mediated nociceptive reflexes. Bilateral N-methyl-D-aspartate
(NMDA)-induced lesions of the rat Ce, but not bilateral lesions centered on
either the basolateral or medial amygdaloid nucleus, abolished the
antinociception produced by 2.5 mg/kg morphine sulfate in the noxious
heat-evoked tail-flick test. Bilateral Ce lesions also abolished the
antinociception produced by 2 or 4 mg/kg morphine sulfate, but a relatively
large dose of morphine sulfate (10 mg/kg, s.c.) resulted in partial
reinstatement of antinociception. It is unlikely that these effects were
due to secondary, seizure-induced damage following NMDA injection (e.g., to
areas outside the amygdala) since bilateral inactivation of the Ce with the
local anesthetic lidocaine also reliably attenuated morphine
antinociception. It is also unlikely that these effects were artifacts of
lesion-induced hyperalgesia, since Ce lesions failed to result in reliable
thermal hyperalgesia, even at baseline tail-flick latencies of 10-12 sec.
These data are the first to provide direct evidence that systemically
administered morphine requires the integrity of a forebrain area in order
to suppress spinally mediated nociceptive reflexes. It is argued that the
present results, together with recent evidence linking the Ce to the
production of several forms of conditioned and unconditioned
environmentally induced antinociception, warrant incorporation of the Ce
into current models of endogenous pain control circuitry.
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