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对于精神分裂症的生物学基本病因机制仍是不甚明瞭的。近30年来,关于精神分裂症的多巴胺假说获得了药理学试验的依据。近来,已从细胞学和分子生物学水平上开展了对分裂症病人多巴胺活性的直接研究。Farle等Crow等及Bird等(1979)先后报告在分裂症病人的脑尸检标本中发现中隔腹侧纹状体及伏核中多巴胺浓度明显增高。Ma Ckay(1982)报告,年轻的分裂症病人尾状核和伏核的多巴胺浓度显著高于同性别同年龄的对照组。在活体中直接观察脑中多巴胺活性的变化是不可能的,而间接地通过测定血清垂体激素来观察多巴胺活性变化则是可能的。多巴胺具有抑制促甲状腺释放激素(TRH)、促甲状腺素(TSH)和催乳素释放的作用。
The basic aetiological mechanism of schizophrenia remains unclear. For nearly 30 years, the dopamine hypothesis on schizophrenia has gained the basis of pharmacological tests. Recently, direct studies of dopamine activity in patients with schizophrenia have been conducted at cytology and molecular biology level. Farle et al., Crow et al., And Bird et al. (1979) reported that in the autopsy specimens of patients with schizophrenia, the septum ventral striatum and dopamine concentration in the nucleus accumbens were significantly increased. Ma Ckay (1982) reported that young patients with schizophrenia had significantly higher dopamine concentrations in the caudate and nucleus accumbens than controls of the same sex and age. It is not possible to directly observe changes in dopamine activity in the brain in vivo, whereas it is possible to observe changes in dopamine activity indirectly by measuring serum pituitary hormones. Dopamine has the effect of inhibiting thyrotropin-releasing hormone (TRH), thyrotropin (TSH) and prolactin release.