Pentobarbital induces nocifensive hyperreflexia, not hyperalgesia in rats

Purpose: To seek behavioural, reflexive and histochemical evidence of long- lasting changes in nociceptive stimulus transmission induced by exposure to doses of pentobarbital that induce nocifensive hyperreflexia. Methods: Nocifensive hyperreflexia was induced in 12 rats with 30 mg(.)kg(- 1) pentobarbital ip. Reflex latency times for withdrawal of the hind paw fr om noxious radiant heat were measured with an automated electronic timer. S ubjective responses to noxious stimulation (licking or biting of the stimul ated hindpaw) and the level of sedation were recorded. Histological section s of lumbar spinal cord were stained for immunoreactivity of the immediate- early-gene (IEG), c-ibs, in three rats that received repeated threshold nox ious radiant heat stimulation during the period of nocifensive hyperreflexi a induced by 30 mg(.)kg(-1) pentobarbital ie. Results: Reflex withdrawal latency decreased by 32 +/- 8% of control values (P < 0.001) following pentobarbital injection and returned to control valu es 120 min after drug injection. Once fully alert, pentobarbital-treated an imals did not show any increase in nociceptive behaviour relative to saline -injected controls (P = 0.41). Sustained noxious stimulation to the hindpaw in halothane-anesthetized animals was associated with an increase in c-fos immunoreactivity in the dorsal horn of the lumbar spinal cord ipsilateral to the stimulation (P < 0.001). Threshold stimulation in the pentobarbital- treated animals was not associated with any increase in c-fos expression. Conclusions: During pentobarbital-induced hyperreflexia, rats did not show any reflexive, behavioural, or histochemical evidence of long-lasting enhan cement of nocifensive signal transmission. The results are consistent with previous observations that, in the absence of tissue injury, nocifensive hy perreflexia induced by barbiturates is a short-lived pharmacological effect .