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The present study investigated the role of somatodendritic 5-HT1A autoreceptors located in the dorsal and median raphe nuclei on the stimulant effect of cocaine on locomotor activity, rears and head bobs in female Glaxo Wistar rats. Cocaine was administered at a submaximal dose of 15 mg/kg i.p. to enable either a potentiation or attenuation to be observed. The selective 5-HT1A antagonist WAY100635 (0.21 ng or 21 ng) or saline was microinjected in the dorsal or median raphe nuclei followed by the peripheral administration of cocaine 60 min later. WAY 100635 microinjected in the dorsal or median raphe nuclei did not consistently alter the locomotor activity and the number of rears of saline-treated animals. Microinjection of WAY100635 in the dorsal raphe nucleus potentiated cocaine-induced locomotor activity and the number of head bobs. The number of rears induced by cocaine was not significantly altered by WAY100635 microinjected in the dorsal raphe nucleus. In contrast, microinjection of WAY100635 in the median raphe nucleus did not alter the stimulant effect of cocaine on locomotor activity, rears or head bobs. It may be suggested from these results that stimulation of somatodendritic 5-HT1A autoreceptors located in the dorsal raphe nucleus mediates an inhibitory effect on cocaine-induced locomotor activity and head bobs, whereas somatodendritic 5-HT1A autoreceptors in the median raphe nucleus are not involved in the inhibitory role of 5-HT on the stimulant effect of cocaine on locomotor activity and head bobs. A differential involvement of the midbrain raphe nuclei may exist controlling the stimulant effect of cocaine on locomotor activity and head bobs.

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1 The present study investigated the central e ects of the selective serotonin reuptake inhibitor (SSRI)¯uoxetine and the role of 5-hydroxytryptamine 3 (5-HT 3 ) receptors in the core of the nucleus accumbens (NAc) on cocaine-induced behavioural changes in rats. 2 The 5-HT 3 receptor antagonist ondansetron (1 or 10 ng) was microinjected bilaterally into the core of the NAc 60 min prior to peripheral cocaine (15 mg kg 71 , i.p.) administration followed by the assessment of locomotor activity, rearing activity and head bobs. Both doses of ondansetron attenuated cocaine's stimulatory e ect on behaviours. 3 Fluoxetine (0.05 or 5 mg) microinjected bilaterally into the core of the NAc 30 min before peripheral administration of cocaine produced dose-dependent biphasic e ects on cocaine-induced behaviours. Intra-NAc administration of 0.05 mg¯uoxetine resulted in a potentiation of cocaineinduced behaviours, while the higher dose of the SSRI (5 mg) attenuated the stimulant e ect of cocaine on behaviours. 4 To investigate a possible involvement of 5-HT 3 receptors in¯uoxetine's facilitatory action, ondansetron (10 ng) was microinjected 30 min prior to¯uoxetine (0.05 mg), which resulted in a signi®cant attenuation of the facilitatory e ect of¯uoxetine on cocaine-induced behaviours. 5 Thus, 5-HT 3 receptors in the core of the NAc appear to mediate stimulatory e ects on cocaineinduced locomotor activity, rears and head bobs, whereas the attenuation of cocaine-induced behaviours by¯uoxetine at the higher dose, suggests the involvement of a di erent 5-HT receptor subtype.

No abstract