Administration of the 5-HT releasing agent, fenfluramine, to rats produced decreases in food intake and locomotor activity, and increases in plasma prolactin and corticosterone concentrations. Short-term but not long-term treatment with lithium (antimanic and antidepressant agent) potentiated fenfluramine-induced suppression of food intake but not locomotor activity. Short-term treatment with lithium but not clorgyline (MAO type A inhibiting antidepressant) or imipramine (a tricyclic antidepressant) potentiated fenfluramine-induced increases in plasma prolactin but not on corticosterone. These findings indicate that various agents effective in different types of affective disorders exert differential modulatory influences on serotonergic mechanisms regulating food intake, locomotor activity and neuroendocrine changes in vivo. In another study, acute pretreatment with various doses of m- chlorophenylpiperazine (m-CPP, 5-HT1 agonist) attenuated 8-hydroxy-2(di-N- propylamino tetralin (8-OH-DPAT, 5-HT1A agonist)-induced increases in food intake in the free-feeding paradigm and enhanced 8-OH-DPAT-induced decreases in food intake in the food-deprived paradigm. In the two paradigms, however, neither increases nor decreases in food intake induced by 8-OH-DPAT were altered in animals following long-term (21-day) treatment with m-CPP vs. saline when animals were challenged with 8-OH-DPAT after 48 hr after the last dose of m-CPP. These findings suggest that long-term m- CPP treatment does not alter the functional sensitivity of 5-HT1A receptors located presynaptically that mediate hyperphagia or 5-HT1A receptors located post-synaptically that medicate decreases in food intake by induction of the serotonin behavioral syndrome.
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