Increased striatal dopamine transmission in schizophrenia: confirmation in a second cohort.

Increased striatal dopamine transmission in schizophrenia: confirmation in a second cohort.
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DOI:
10.1176/ajp.155.6.761
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发表时间:
1998-06
期刊:
The American journal of psychiatry
影响因子:
--
通讯作者:
A. Abi-Dargham;R. Gil;J. Krystal;R. Baldwin;J. Seibyl;M. Bowers;C. Dyck;D. Charney;R. Innis;M. Laruelle
A. Abi-Dargham;R. Gil;J. Krystal;R. Baldwin;J. Seibyl;M. Bowers;C. Dyck;D. Charney;R. Innis;M. Laruelle
中科院分区:
其他
文献类型:
--
作者:
A. Abi-Dargham;R. Gil;J. Krystal;R. Baldwin;J. Seibyl;M. Bowers;C. Dyck;D. Charney;R. Innis;M. Laruelle

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作者先前观察到15名未治疗的精神分裂症患者与15名匹配的健康受试者相比,在安非他明刺激后纹状体多巴胺传递增加。这项研究的目的是在一组新的精神分裂症患者和健康受试者中重复这一发现。方法招募15名精神分裂症患者和15名年龄、性别、种族和父母社会经济地位相匹配的健康受试者。患者符合精神分裂症的DSM-IV标准,无酒精或药物滥用或依赖史,至少21天无抗精神病药。通过急性安非他明刺激(0.3 mg/kg,静脉注射)引起多巴胺D2受体可用性降低来评估安非他明诱导的多巴胺释放。用单光子发射计算机断层扫描和D2受体放射性示踪剂[123I]IBZM测量D2受体可用性的降低。结果精神分裂症患者与对照组在D2受体可用性基线上无差异。与对照组相比,精神分裂症患者在急性安非他明刺激后D2受体可用性明显降低。在本研究中,效应量小于第一次研究。过量的多巴胺释放与安非他明后阳性症状的短暂出现或恶化有关。结论:在这个新的研究队列中,作者重复了他们最初对精神分裂症患者纹状体多巴胺释放失调的观察。
OBJECTIVE The authors previously observed an increase in striatal dopamine transmission following amphetamine challenge in 15 untreated patients with schizophrenia compared to 15 matched healthy subjects. The purpose of this study was to replicate this finding in a new cohort of schizophrenic patients and healthy subjects. METHOD Fifteen patients with schizophrenia and 15 healthy subjects matched for age, gender, ethnicity, and parental socioeconomic status were recruited for this study. Patients fulfilled DSM-IV criteria for schizophrenia, had no history of alcohol or substance abuse or dependence, and were neuroleptic free for a minimum of 21 days. Amphetamine-induced dopamine release was assessed by the reduction in dopamine D2 receptor availability induced by an acute amphetamine challenge (0.3 mg/kg, intravenous bolus). Reduction in D2 receptor availability was measured with single photon emission computed tomography and the D2 receptor radiotracer [123I]IBZM. RESULTS No differences were observed between patients with schizophrenia and the comparison group in D2 receptor availability at baseline. Patients with schizophrenia exhibited a significantly larger reduction in D2 receptor availability following acute amphetamine challenge than the comparison group. In this study, the effect size was smaller than in the first study. Excess dopamine release following amphetamine was associated with transient emergence or worsening of positive symptoms. CONCLUSIONS In this new cohort of subjects the authors replicated their initial observation of a dysregulation of striatal dopamine release in schizophrenia.