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The aim of this study was to investigate the effects of cocaine on tachykinin-mediated pain transmission in the rat spinal cord in vivo using a single pungent stimulus. The first part of this study showed that intrathecal (i.t.) pretreatment with the tachykinin NK(1) receptor antagonist L-703,818 (20, 50, 100 microg) lowered the nociceptive response induced by i.t. substance P (NK(1) receptor agonist) in a dose-dependent manner. In the second part of this study, the effects of cocaine (20 mg/kg, i.p.) were investigated on the pain response induced by i.t. substance P (100 microg) in the presence of L-703,818 (50 microg, i.t.) in rats. Cocaine enhanced the nociceptive response induced by i.t. substance P, indicating that cocaine potentiates tachykinin-mediated pain transmission. The effects of cocaine were counteracted by i.t. pretreatment with the cocaine-metabolizing enzyme inhibitor debrisoquine (10, 20, 40, 80 mg/kg, i.p.), but not by i.p. pretreatment with L-703,818. The results suggest that cocaine increases the nociceptive response induced by i.t. substance P in the spinal cord in vivo. This effect seems to be related to enhanced production of the tachykinin NK(1) receptor-mediated neurotransmitter as indicated by the inhibition produced by L-703,818, but not by cocaine-metabolizing enzyme inhibition. the shrinkage of the church and the growth of the international community of the Beatitudes.
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