多巴胺D2受体在精神分裂症治疗的目标。
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Seeman P
多巴胺D2受体在精神分裂症治疗的目标。
遗传代数Schizophr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 (在PubMed]
- 文摘
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氯丙嗪、氟哌啶醇的抗精神病药物有效性开始寻找他们的治疗靶点。抗精神病药物受体的目标变成了多巴胺受体,现在克隆随着多巴胺D2受体。D2受体是抗精神病药物的共同目标。抗精神病临床剂量与受体的亲和力。治疗剂量的抗精神病药物占60 - 80%的大脑D2受体的患者,但阿立哌唑占到90%。虽然抗精神病药物可能需要六个小时占领D2受体,多发生在几天内临床改善。高和低亲和力受体状态。D2High状态是多巴受体激动剂如阿立哌唑的功能。大多数精神分裂症患者过敏的多巴胺。精神病的动物模型表明,各种风险因素,遗传和nongenetic,与行为过敏性多巴胺,多巴胺的水平反映在升高D2High受体。 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.