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胎儿期受辐射的非人灵长类动物的颅面畸形发生:对精神分裂症神经发育假说的启示。

Craniofacial dysmorphogenesis in fetally irradiated nonhuman primates: implications for the neurodevelopmental hypothesis of schizophrenia.

作者信息

Gelowitz Douglas L, Rakic Pasko, Goldman-Rakic Patricia S, Selemon Lynn D

机构信息

Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.

出版信息

Biol Psychiatry. 2002 Oct 1;52(7):716-20. doi: 10.1016/s0006-3223(02)01380-x.

DOI:10.1016/s0006-3223(02)01380-x
PMID:12372662
Abstract

BACKGROUND

Craniofacial abnormalities arising from gestational disturbances have been documented in some schizophrenic patients. Reduction of thalamic neurons, a key feature of the neuropathology of schizophrenia, could also have a prenatal origin via disruption of thalamic neurogenesis. This study investigates whether craniofacial dysmorphology and thalamic neuron loss might be associated manifestations of a disruption in embryonic development.

METHODS

Thalamic neurons were deleted by exposing fetal macaques to x-rays during thalamic genesis (E33-42). Another group of macaques was irradiated after thalamic genesis (E70-81). Body, head, and facial measurements were obtained from the early irradiated (EX), late irradiated (LX), and control animals at adulthood.

RESULTS

Head width, distance between outer eye edges, and ear width were smaller in EX macaques compared with control animals. The LX macaques exhibited only reduced ear width compared with control animals.

CONCLUSIONS

These findings indicate that certain features of thalamic neuropathology and craniofacial dysmorphogenesis observed in schizophrenic patients may have a common etiology.

摘要

背景

在一些精神分裂症患者中已记录到由妊娠紊乱引起的颅面异常。丘脑神经元减少是精神分裂症神经病理学的一个关键特征,它也可能通过丘脑神经发生的破坏而起源于产前。本研究调查颅面畸形和丘脑神经元丢失是否可能是胚胎发育中断的相关表现。

方法

在丘脑发生期(E33 - 42)将胎猴暴露于X射线下以删除丘脑神经元。另一组猕猴在丘脑发生期之后(E70 - 81)接受照射。在成年期从早期照射组(EX)、晚期照射组(LX)和对照动物获取身体、头部和面部测量数据。

结果

与对照动物相比,EX猕猴的头宽、外眼角间距和耳宽较小。与对照动物相比,LX猕猴仅表现出耳宽减小。

结论

这些发现表明,在精神分裂症患者中观察到的丘脑神经病理学和颅面畸形发生的某些特征可能有共同的病因。

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