Noradrenergic and serotonergic involvement in brief shock-induced analgesia in rats.

Four experiments were performed to investigate the effects of different techniques causing noradrenergic and serotonergic depletions in the brain and spinal cord on brief shock-induced analgesia. Newborn pups were administered N-2-choloroethyl-N-ethyl-2-bromobenzylamine systemically (2 x 50 mg/kg, ip) and 6-hydroxydopamine administered either systemically (100 micrograms/g, sc) or directly (8 micrograms in 1 microliter, bilaterally) into the locus coeruleus region, or intrathecally (20 micrograms in 10 microliter) into the lumbar subarachnoidal space, caused notable and consistent attenuations of the analgesia caused by brief shock. These treatments reduced noradrenaline concentrations in the spinal cord drastically. A potentiation of brief shock-induced analgesia was caused by the administration of p-chlorophenyl-alanine, whereas administration of 5,7-dihydroxytryptamine, into the nucleus raphe magnus or intrathecally into the subarachnoidal space, produced attenuation of the analgesic effect. Biochemical analyses revealed marked 5-hydroxytryptamine depletions in the spinal cord. The present findings are discussed with regard to the role of spinal noradrenaline and 5-hydroxytryptamine involvement in brief shock-induced analgesia and in reactions to stressful events.