多巴胺D2受体是精神分裂症的治疗靶点。
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Seeman P
多巴胺D2受体是精神分裂症的治疗靶点。
临床精神分裂症相关精神病。2010年4月4(1):56-73。doi: 10.3371 / CSRP.4.1.5。
- PubMed ID
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20643630 (查看PubMed］
- 摘要
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氯丙嗪和氟哌啶醇的抗精神病效果开始寻找它们的治疗靶点。必威国际app抗精神病受体靶点原来是多巴胺受体，现在被克隆为多巴胺D2受体。D2受体是抗精神病药物的共同靶点。抗精神病药物的临床剂量与其对该受体的亲和力有关。治疗剂量的抗精神病药物占据患者大脑中60 - 80%的D2受体，但阿立哌唑占据高达90%。虽然抗精神病药物可能需要6个小时才能占据D2受体，但在几天内就会有很大的临床改善。受体有高亲和和低亲和状态。D2High状态对阿立哌唑等多巴胺样激动剂有作用。大多数精神分裂症患者对多巴胺超敏感。精神病的动物模型表明，遗传和非遗传的多种风险因素与多巴胺的行为超敏有关，反映在多巴胺D2High受体的升高水平上。 Although antipsychotics such as haloperidol alleviate psychosis and reverse the elevation of D2High receptors, long-term use of traditional antipsychotics can further enhance dopamine supersensitivity in patients. Therefore, switching from a traditional antipsychotic to an agonist antipsychotic such as aripiprazole can result in the emergence of psychotic signs and symptoms. Clozapine and quetiapine do not elicit parkinsonism and rarely result in tardive dyskinesia because they are released from D2 within 12 to 24 hours. Traditional antipsychotics remain attached to D2 receptors for days, preventing relapse, but allowing accumulation that can lead to tardive dyskinesia. Future goals include imaging D2High receptors and desensitizing them in early-stage psychosis.