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A feedforward inhibitory circuit mediates lateral refinement of sensory representation in upper layer 2/3 of mouse primary auditory cortex.
自闭症谱系障碍的症状前生物学、结构和功能诊断生物标志物
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Autism.自闭症。
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自闭症动物模型初级听觉皮层中的加工障碍

Impaired Processing in the Primary Auditory Cortex of an Animal Model of Autism.

作者信息

Anomal Renata Figueiredo, de Villers-Sidani Etienne, Brandão Juliana Alves, Diniz Rebecca, Costa Marcos R, Romcy-Pereira Rodrigo N

机构信息

Brain Institute, Federal University of Rio Grande do Norte Natal, Brazil.

Montreal Neurological Institute, McGill University Montreal, QC, Canada.

出版信息

Front Syst Neurosci. 2015 Nov 16;9:158. doi: 10.3389/fnsys.2015.00158. eCollection 2015.

DOI:10.3389/fnsys.2015.00158
PMID:26635548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4644803/
Abstract

Autism is a neurodevelopmental disorder clinically characterized by deficits in communication, lack of social interaction and repetitive behaviors with restricted interests. A number of studies have reported that sensory perception abnormalities are common in autistic individuals and might contribute to the complex behavioral symptoms of the disorder. In this context, hearing incongruence is particularly prevalent. Considering that some of this abnormal processing might stem from the unbalance of inhibitory and excitatory drives in brain circuitries, we used an animal model of autism induced by valproic acid (VPA) during pregnancy in order to investigate the tonotopic organization of the primary auditory cortex (AI) and its local inhibitory circuitry. Our results show that VPA rats have distorted primary auditory maps with over-representation of high frequencies, broadly tuned receptive fields and higher sound intensity thresholds as compared to controls. However, we did not detect differences in the number of parvalbumin-positive interneurons in AI of VPA and control rats. Altogether our findings show that neurophysiological impairments of hearing perception in this autism model occur independently of alterations in the number of parvalbumin-expressing interneurons. These data support the notion that fine circuit alterations, rather than gross cellular modification, could lead to neurophysiological changes in the autistic brain.

摘要

自闭症是一种神经发育障碍,临床特征为沟通缺陷、缺乏社交互动以及伴有兴趣受限的重复行为。多项研究报告称,感觉知觉异常在自闭症个体中很常见,可能导致该障碍复杂的行为症状。在这种情况下,听觉不一致尤为普遍。鉴于这种异常处理可能部分源于脑回路中抑制性和兴奋性驱动的失衡,我们使用了孕期丙戊酸(VPA)诱导的自闭症动物模型,以研究初级听觉皮层(AI)的音频定位组织及其局部抑制性回路。我们的结果表明,与对照组相比,VPA大鼠的初级听觉图谱发生扭曲,高频过度代表,感受野广泛调谐,声音强度阈值更高。然而,我们未检测到VPA大鼠和对照大鼠AI中小清蛋白阳性中间神经元数量的差异。总之,我们的研究结果表明,该自闭症模型中听觉感知的神经生理损伤独立于表达小清蛋白的中间神经元数量的改变而发生。这些数据支持这样一种观点,即精细的回路改变而非总体细胞修饰可能导致自闭症大脑中的神经生理变化。

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