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J Neurodev Disord. 2009 Jun;1(2):172-81. doi: 10.1007/s11689-009-9023-x. Epub 2009 Jul 11.

Common circuit defect of excitatory-inhibitory balance in mouse models of autism.

Abstract

One unifying explanation for the complexity of Autism Spectrum Disorders (ASD) may lie in the disruption of excitatory/inhibitory (E/I) circuit balance during critical periods of development. We examined whether Parvalbumin (PV)-positive inhibitory neurons, which normally drive experience-dependent circuit refinement (Hensch Nat Rev Neurosci 6:877-888, 1), are disrupted across heterogeneous ASD mouse models. We performed a meta-analysis of PV expression in previously published ASD mouse models and analyzed two additional models, reflecting an embryonic chemical insult (prenatal valproate, VPA) or single-gene mutation identified in human patients (Neuroligin-3, NL-3 R451C). PV-cells were reduced in the neocortex across multiple ASD mouse models. In striking contrast to controls, both VPA and NL-3 mouse models exhibited an asymmetric PV-cell reduction across hemispheres in parietal and occipital cortices (but not the underlying area CA1). ASD mouse models may share a PV-circuit disruption, providing new insight into circuit development and potential prevention by treatment of autism.

ELECTRONIC SUPPLEMENTARY MATERIAL:

The online version of this article (doi:10.1007/s11689-009-9023-x) contains supplementary material, which is available to authorized users.

KEYWORDS:

GABA; Neuroligin; Parvalbumin; VPA

PMID:
20664807
[PubMed]
PMCID:
PMC2906812
Free PMC Article
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