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Journal of Neuroscience, Vol 11, 1433-1439, Copyright © 1991 by Society for Neuroscience
Hyperalgesia during acute opioid abstinence: evidence for a nociceptive facilitating function of the rostral ventromedial medulla
H Kaplan and HL Fields
Department of Neurology, University of California, San Francisco 94143.
Naloxone-precipitated opioid abstinence is associated with enhancement of
reflex responses to noxious stimulation (hyperalgesia). The present
experiments in lightly anesthetized rats were designed to determine (1)
whether neurons in the rostral ventromedial medulla (RVM) contribute to
this enhancement, and (2) whether this enhancement is due to removal of an
inhibitory modulatory influence or to activation of a facilitatory
influence. In the first experiment, 10 micrograms of morphine was
microinjected into the RVM; subsequent administration of naloxone (1 mg/kg,
i.v.) shortened tail-flick latency. This is evidence that a synaptic action
of opioids within the RVM can contribute to hyperalgesia. In the second
experiment, systemic administration of morphine (2 mg/kg, i.v.) was
followed by systemic administration of naloxone (1 mg/kg, i.v.), which
produced a significant hyperalgesia that could be markedly attenuated by
microinjection of 10 micrograms lidocaine into the RVM. That inactivation
of RVM reduces the hyperalgesia indicates that the CNS is capable of
generating a facilitating action on nociceptive transmission. Previous
studies from this laboratory have indicated that a population of RVM
neurons, on- cells, shows increased activity during opioid abstinence. The
present experiments support the hypothesis that RVM on-cells exert a
facilitating influence on nociceptive transmission.
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