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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Increased m-CPP-induced oral dyskinesia after lesion of serotonergic neurons.
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Increased m-CPP-induced oral dyskinesia after lesion of serotonergic neurons.

机译：血清素能神经元病变后m-CPP引起的口腔运动障碍增加。

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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.
机译：5-羟基色胺（5-HT）（2C / 1B）激动剂1-（间氯苯基）哌嗪（m-CPP）的外周给药会在大鼠中产生异常的口腔运动。我们以前已经表明，这种行为是由丘脑下核中的5-HT（2C）受体介导的[Neuroscience 72（1996）117]。本研究检查了5-羟色胺耗竭后的这种作用，以确定去除内源性5-羟色胺是否影响了这种行为反应和/或丘脑下5-HT（2C）受体。大鼠在接受去甲丙胺预处理（25 mg / kg ip）后，接受脑室内的神经毒素5,7-二羟基色胺（5,7-DHT，100 mg / 10 ml）或赋形剂输注。通过放射自显影测定的5-羟色胺摄取部位的减少证实了5-羟色胺耗竭的功效。与假手术的对照组相比，在假手术的第4天和第8天，由m-CPP（1.0 mg / kg ip ip）外周给药引起的口腔运动障碍明显增加，而在假手术后第12天则没有。注射m-CPP后表现出短暂性癫痫发作的一部分病变大鼠在观察期间没有阻止口腔运动障碍的测量。在5,7-DHT损伤后5天处死的大鼠中，丘脑下核或其他表达该受体的脑区域中的配体结合放射自显影未发现5-HT（2C）受体水平的差异。数据表明，成年大鼠中的血清素能神经元病变诱导了由丘脑下5-HT（2C）受体介导的运动反应的短暂增加。这些数据表明，丘脑下核中5-羟色胺能传递的功能改变可能与运动亢进性疾病的病理生理有关。

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