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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Reversal of haloperidol-induced tardive vacuous chewing movements and supersensitive somatodendritic serotonergic response by buspirone in rats.
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Reversal of haloperidol-induced tardive vacuous chewing movements and supersensitive somatodendritic serotonergic response by buspirone in rats.

机译：丁螺环酮逆转氟哌啶醇诱导的迟发性空泡咀嚼运动和超敏性树突状血清素能反应。

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摘要

Tardive dyskinesia (TD), a syndrome of involuntary hyperkinesias in the orofacial region that develops in patients chronically treated with neuroleptic agents is a major limitation of the therapy. Rats chronically treated with haloperidol exhibit vacuous chewing movements (VCMs) with the twitching of facial musculature and tongue protrusion. The syndrome is widely used as an animal model of TD. Evidence suggests a role of 5-hydroxytryptamine (5-HT; serotonin)-1A receptors in the pathogenesis and treatment of TD because repeated administration of haloperidol resulted in an increase in the effectiveness of 5-HT-1A receptors while drugs with agonist activity at 5-HT-1A receptors could attenuate haloperidol-induced VCMs. The present study was designed to test the hypothesis that a decrease in the responsiveness of somatodendritic 5-HT-1A receptors by the coadministration of buspirone could reverse the induction of VCMs and supersensitivity at 5-HT-1A receptors by haloperidol. Rats treated with haloperidol at a dose of 1 mg/kg twice a day for 2 weeks displayed VCMs with twitching of facial musculature that increased in a time dependent manner as the treatment continued to 5 weeks. Coadministration of buspirone attenuated haloperidol-induced VCMs after 2 weeks and completely prevented it after 5 weeks. The intensity of 8-hydroxy-2-di (n-propylamino) tetralin (8-OH-DPAT)-induced locomotion was greater in saline+haloperidol injected animals but not in buspirone+haloperidol injected animals. 8-OH-DPAT-induced decreases of 5-HT metabolism were greater in saline+haloperidol injected animals but not in buspirone+haloperidol injected animals. It is suggested that an impaired somatodendritic 5-HT-1A receptor dependent response is a major contributing factor in the pathophysiology of TD and a normalization of the somatodendritic response by drugs may help extending therapeutics in schizophrenia.
机译：迟发性运动障碍（TD）是一种在口部区域发生的非自愿性运动过度综合征，这种疾病在用精神安定药长期治疗的患者中发展，是该疗法的主要局限性。长期用氟哌啶醇治疗的大鼠表现出空腹的咀嚼运动（VCM），且伴有面部肌肉组织和舌头突出处的抽搐。该综合征被广泛用作TD的动物模型。有证据表明5-羟色胺（5-HT; 5-羟色胺）-1A受体在TD的发病机理和治疗中的作用，因为氟哌啶醇的重复给药导致5-HT-1A受体的效力增加，而激动剂在5-HT-1A受体可以减弱氟哌啶醇诱导的VCM。本研究旨在检验以下假说：并用丁螺环酮降低体树突状5-HT-1A受体的反应性可以逆转氟哌啶醇对VCM的诱导和对5-HT-1A受体的超敏性。每天两次用氟哌啶醇以1 mg / kg的剂量治疗的大鼠持续2周，表现出VCM伴面部肌肉抽搐，随着治疗持续5周，其呈时间依赖性增加。 2周后并用丁螺环酮减毒氟哌啶醇诱导的VCM，5周后完全预防。在生理盐水+氟哌啶醇注射的动物中，由8-羟基-2-二（正丙基氨基）四氢化萘（8-OH-DPAT）诱导的运动强度更大，而在丁螺环酮+氟哌啶醇注射的动物中，运动强度更大。 8-OH-DPAT诱导的5-HT代谢减少在盐水+氟哌啶醇注射的动物中更大，而在丁螺环酮+氟哌啶醇注射的动物中则没有。提示受损的树突状5-HT-1A受体依赖性反应是TD病理生理的主要促成因素，药物使树突状反应正常化可能有助于扩大精神分裂症的治疗方法。

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