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  • Title: Role of postsynaptic serotonin1A receptors in risperidone-induced increase in acetylcholine release in rat prefrontal cortex.
    Author: Sato M, Ago Y, Koda K, Nakamura S, Kawasaki T, Baba A, Matsuda T.
    Journal: Eur J Pharmacol; 2007 Mar 22; 559(2-3):155-60. PubMed ID: 17258195.
    Abstract:
    Most atypical antipsychotic drugs increase acetylcholine release in the prefrontal cortex, but the detailed mechanism is still unknown. The present study examined the role of serotonin (5-HT)1A receptors in risperidone-induced increases in acetylcholine release in rat prefrontal cortex. Systemic administration of risperidone at doses of 1 and 2 mg/kg increased acetylcholine release in the prefrontal cortex in a dose-dependent manner. This increase was antagonized by systemic administration of high doses (1 and 3 mg/kg) of N-{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}-N-(2-pyridinyl)cyclohexanecarboxamide (WAY100635), a 5-HT1A receptor antagonist/dopamine D4 receptor agonist, but not by a low dose (0.1 mg/kg) of the antagonist which antagonizes preferentially presynaptic 5-HT1A autoreceptors. Furthermore, local application of WAY100635 into the prefrontal cortex also attenuated risperidone-induced increases in acetylcholine release. WAY100635 alone did not affect acetylcholine release in the prefrontal cortex. On the other hand, local application of risperidone (3 and 10 microM), the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (1 and 10 microM), and the dopamine D4 receptor antagonist 3-(4-(4-iodophenyl)piperazine-1-yl)methyl-1H-pyrrolo[2,3-b]pyridine (1 and 10 microM) into the cortex did not affect acetylcholine release in the prefrontal cortex. These results suggest that risperidone increases acetylcholine release in the prefrontal cortex through a complex mechanism which is enhanced by prefrontal 5-HT1A receptor activation.
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