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A new paradigm for understanding gamma-aminobutyric acid cell pathology in schizophrenia?

机译:在精神分裂症中理解γ-氨基丁酸细胞病理学的新范式?

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摘要

The article by Joshi et al. (1) in this edition of Biological Psychiatry is a provocative study that addresses a long-standing question as to whether gamma-aminobutyric acid (GABA) cell pathology in schizophrenia can be understood within a neuro-developmental framework. Following initial reports that GABA cells are reduced in number and function in superficial cortical layers in schizophrenics, it was suggested that these changes may be related to disturbed migration during prenatal and early postnatal development (2). Ted Jones and his colleagues provided support for this hypothesis by demonstrating that a reduced density of presumptive intemeurons in superficial layers of prefrontal cortex was accompanied by a significant increase in the number of these cells in the subcortical white matter (3).
机译:Joshi等人的文章。 (1)在本版生物精神病学中,是一种挑衅性的研究,可以解决精神分裂症中γ-氨基丁酸(GABA)细胞病理是否可以在神经发育骨架内理解。 在初步报告之后,在精神分裂症中的浅表皮层层中的数量和功能下降,提示这些变化可能与产前和早期产前发育期间的迁移有关(2)。 泰德琼斯及其同事通过证明前额叶皮质浅层皮质浅层皮层中的推定内胸的密度降低,伴随着皮质片(3)中这些细胞数量的显着增加,为该假设提供了对该假设的支持。

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