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

被引:41
|
作者
Golden, Carla E. M. [1 ,2 ,3 ]
Buxbaum, Joseph D. [1 ,2 ,3 ,4 ,5 ]
De Rubeis, Silvia [1 ,2 ]
机构
[1] Icahn Sch Med Mt Sinai, Seaver Autism Ctr Res & Treatment, 1468 Madison Ave, New York, NY 10029 USA
[2] Icahn Sch Med Mt Sinai, Dept Psychiat, 1468 Madison Ave, New York, NY 10029 USA
[3] Icahn Sch Med Mt Sinai, Friedman Brain Inst, 1468 Madison Ave, New York, NY 10029 USA
[4] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, 1468 Madison Ave, New York, NY 10029 USA
[5] Icahn Sch Med Mt Sinai, Mindich Child Hlth & Dev Inst, 1468 Madison Ave, New York, NY 10029 USA
关键词
PHELAN-MCDERMID SYNDROME; DEEP BRAIN-STIMULATION; CORTICOSTRIATAL CONNECTIVITY; SYNAPTIC STRENGTH; CRITICAL-PERIOD; MATURATION; SYNGAP1; MECP2; DYSFUNCTION; MECHANISMS;
D O I
10.1016/j.conb.2017.11.006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:106 / 112
页数:7
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