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The function of the 5-hydroxytryptamine (5-HT) system in the medial vestibular nucleus (MVN) was evaluated using KCl-evoked 5-HT release assessed by in vivo microdialysis. The release of 5-HT in the MVN was increased by the local application of KCl (100 mM) in a calcium-dependent manner. Likewise, perfusion of a 5-HT reuptake blocking agent, clomipramine (1 microM), increased extracellular levels of 5-HT in the MVN. Finally, pretreatment with the selective 5-HT(1A) agonist, 8-hydroxy-2-(di-N-propylamino) tetralin (1 mg/kg, intraperitoneally), attenuated the KCl-evoked 5-HT release. These findings suggest that 5-HT stored in vesicles is released from nerve terminals in the MVN. In addition, its regulation may be mediated by control of somatodendritic 5-HT(1A) receptor activation.

The behavioral and neurochemical effects of high doses of amphetamine administered to BALB/c mice were examined in the presence and absence of co-administered haloperidol (a D2 antagonist), SCH 23390 (a D1 antagonist) and risperidone (a mixed 5-HT2/D2 antagonist). It was observed that mice displayed a dose-dependent increase in stereotypic behavior, oral dyskinesia, and self-injurious behavior (SIB) in response to amphetamine treatment. Furthermore, agents that blocked the SIB reversed the amphetamine-induced release of serotonin. This effect was unrelated to hyperthermia or non-specific sedation (as assessed by measurement of motor activity). These data are interpreted in the context of the underlying basis of murine SIB involving both dopaminergic and serotonergic activation and demonstrate the efficacy of risperidone in treating these behaviors. [Copyright &y& Elsevier]