Disrupted circuits in mouse models of autism spectrum disorder and intellectual disability.

Disrupted circuits in mouse models of autism spectrum disorder and intellectual disability.
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DOI:
10.1016/j.conb.2017.11.006
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发表时间:
2018-03
影响因子:
5.7
通讯作者:
De Rubeis S
De Rubeis S
中科院分区:
医学2区
文献类型:
--
作者:
Golden CE;Buxbaum JD;De Rubeis S

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自闭症谱系障碍(ASD)和智力残疾(ID)是由广泛的基因突变引起的,其中很大一部分存在于对突触功能重要的基因中。研究发现,在ASD和ID小鼠模型中,感觉区、前额叶区、海马区、小脑区和纹状体区以及连接它们的回路都受到了干扰。解剖这些神经回路中形态和活动的破坏可能有助于我们理解这两种疾病之间的共同风险以及它们的临床异质性。针对这些区域的兴奋和抑制之间的平衡的治疗能够逆转病理表型,阐明这种缺陷是所有模型的共性,并为干预开辟了新的途径。
Autism spectrum disorder (ASD) and intellectual disability (ID) are caused by a wide range of genetic mutations, a significant fraction of which reside in genes important for synaptic function. Studies have found that sensory, prefrontal, hippocampal, cerebellar, and striatal regions, as well as the circuits that connect them, are perturbed in mouse models of ASD and ID. Dissecting the disruptions in morphology and activity in these neural circuits might help us to understand the shared risk between the two disorders as well as their clinical heterogeneity. Treatments that target the balance between excitation and inhibition in these regions are able to reverse pathological phenotypes, elucidating this deficit as a commonality across models and opening new avenues for intervention.
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