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. 1983 Jul;323(3):211-6.
doi: 10.1007/BF00497665.

Effects of intrathecally administered pentobarbital and naloxone on the activity evoked in ascending axons of the rat spinal cord by stimulation of afferent A and C fibres. Further evidence for a tonic endorphinergic inhibition in nociception

Effects of intrathecally administered pentobarbital and naloxone on the activity evoked in ascending axons of the rat spinal cord by stimulation of afferent A and C fibres. Further evidence for a tonic endorphinergic inhibition in nociception

G Bernatzky et al. Naunyn Schmiedebergs Arch Pharmacol. 1983 Jul.

Abstract

The effects of intrathecally administered pentobarbital and naloxone on activity in ascending axons were determined in decerebrate rats with the spinal cord transected at the lower thoracic level. Activity in ascending axons of the spinal cord was recorded below the site of transection and evoked by electrical stimulation of afferent A beta, A delta or C fibres in the sural nerve. Pentobarbital 250 micrograms depressed activity evoked by stimulation of non-nociceptive A beta and nociceptive C fibres; it did not change activity in response to stimulation of A delta fibres. A low dose (100 micrograms) had no effect of A beta and C fibre-evoked activity but depressed spontaneous activity in the ascending axons. Naloxone 5 micrograms enhanced the spontaneous and evoked activities only in those ascending axons which responded to C fibre stimulation. Pretreatment with pentobarbital 250 micrograms prevented the facilitation by naloxone of C fibre-evoked activity. Naloxone was ineffective even when it was administered in a dose of 100 micrograms simultaneously with pentobarbital. Intrathecal injections of magnesium chloride depressed spontaneous and C fibre-evoked activities and markedly reduced the facilitatory effect of naloxone. It is concluded that nociceptive C fibre-evoked activity is subject to the inhibitory control of endorphinergic neurones and that naloxone facilitates this activity by producing release from inhibition.

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