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首页> 外文期刊>World Journal of Neuroscience >“D-cell hypothesis” of schizophrenia: possible theory for mesolimbic dopamine hyperactivity
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“D-cell hypothesis” of schizophrenia: possible theory for mesolimbic dopamine hyperactivity

机译：精神分裂症的“ D细胞假说”：中脑边缘多巴胺亢进的可能理论

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The author proposes a new “D-cell hypothesis” for mesolimbic dopamine (DA) hyperactivity of schizophrenia. The “D-cell” is defined as “non-monoaminergic aromatic L-amino acid decarboxylase (AADC)-containing cell”. D-cells produce trace amines, such as tyramine and β-phenylethylamine, and may also take up amine precursors and convert them to amines by decarboxylation. Trace amine-associated receptor, type 1 (TAAR1), a subtype of trace amine receptors, has a large number of ligands, including tyramine, β-phenylethylamine and methamphetamine, that influence on human mental states, and is now regarded to be a target receptor for novel neuroleptics. Recent studies revealed that the reduced stimulation of TAAR1 on DA neurons in the midbrain ventral tegmental area (VTA) increased firing frequency of VTA DA neurons. The author and her colleagues reported the decrease of D-neurons in the striatum and nucleus accumbens of postmortem brains of patients with schizophrenia. This may imply the decrease of trace amine synthesis, resulting the reduced stimulation of TAAR1 on terminals of midbrain VTA DA neurons, and may lead to mesolimbic DA hyperactivity in schizophrenia. The decrease of striatal D-neurons of postmortem brains of schizophrenia is supposed to be due to neural stem cell dysfunction in the subventricular zone of lateral ventricle. The decrease of striatal D-neurons and acts of TAAR1 signals on DA neurons-might explain mesolimbic DA hyperactivity of schizophrenia.
机译：作者为精神分裂症的中脑边缘多巴胺（DA）过度活跃提出了新的“ D细胞假说”。 “ D细胞”被定义为“含非单胺基芳香族L-氨基酸脱羧酶（AADC）的细胞”。 D细胞产生痕量胺，例如酪胺和β-苯乙胺，并且还可能吸收胺前体，并通过脱羧作用将其转化为胺。痕量胺相关受体1型（TAAR1）是痕量胺受体的一种亚型，具有大量的配体，包括酪胺，β-苯乙胺和甲基苯丙胺，这些配体会影响人类的精神状态，现在被认为是目标新型抗精神病药的受体。最近的研究表明，TAAR1对中脑腹侧被盖区（VTA）中DA神经元的刺激减少，增加了VTA DA神经元的放电频率。作者和她的同事报道了精神分裂症患者死后大脑纹状体和伏隔核中D-神经元的减少。这可能暗示痕量胺合成的减少，导致中脑VTA DA神经元末端对TAAR1的刺激减少，并可能导致精神分裂症的中脑边缘DA过度活跃。精神分裂症的死后脑纹状体D-神经元的减少被认为是由于侧脑室下室神经干细胞功能障碍。纹状体D神经元的减少和TAAR1信号对DA神经元的作用可能解释了精神分裂症的中脑边缘DA过度活跃。

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