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• W2017661577 abstract "Peripheral administration of the 5-hydroxytryptamine (5-HT) 2C/1B agonist 1-( m -chlorophenyl)piperazine ( m -CPP) produces abnormal orofacial movements in rats. We have previously shown that this behavior is mediated by 5-HT 2C receptors in the subthalamic nucleus [Neuroscience 72 (1996) 117]. The present studies examined this effect after serotonin depletion to determine whether removal of endogenous serotonin affected this behavioral response and/or subthalamic 5-HT 2C receptors. Rats received an intraventricular infusion of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, 100 mg/10 ml) or vehicle after desipramine pretreatment (25 mg/kg ip). The efficacy of serotonin depletion was confirmed by a decrease in serotonin uptake sites measured by autoradiography. Oral dyskinesia induced by peripheral administration of m -CPP (1.0 mg/kg ip) was markedly increased in lesioned rats compared to sham-operated controls 4 and 8 but not 12 days after the lesion. A subset of lesioned rats that displayed transient seizures after m -CPP injection did not prevent the measurement of oral dyskinesia during the observation period. No differences in 5-HT 2C receptor levels were found with ligand-binding autoradiography in the subthalamic nucleus, or in other brain regions that express this receptor, in rats sacrificed 5 days following 5,7-DHT lesions. The data indicate that lesion of serotonergic neurons in adult rats induces a transient increase in motor responses mediated by subthalamic 5-HT 2C receptors. These data suggest that functional alterations in serotonergic transmission in the subthalamic nucleus may be involved in the pathophysiology of hyperkinetic movement disorders." @default.
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• W2017661577 date "2001-02-01" @default.
• W2017661577 modified "2023-09-24" @default.
• W2017661577 title "Increased m-CPP-induced oral dyskinesia after lesion of serotonergic neurons" @default.
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• W2017661577 doi "https://doi.org/10.1016/s0091-3057(00)00476-7" @default.
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