Impaired Processing in the Primary Auditory Cortex of an Animal Model of Autism.
Impaired Processing in the Primary Auditory Cortex of an Animal Model of Autism.
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DOI：
10.3389/fnsys.2015.00158
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发表时间：
2015
影响因子：
3
通讯作者：
Romcy-Pereira RN
中科院分区：
文献类型：
--
作者：
Anomal RF;de Villers-Sidani E;Brandão JA;Diniz R;Costa MR;Romcy-Pereira RN
自闭症是一种神经发育障碍，临床特征为沟通缺陷、缺乏社交互动和兴趣受限的重复行为。许多研究报告称，感觉知觉异常在自闭症患者中很常见，并且可能导致该疾病的复杂行为症状。在这种情况下，听力不一致尤其普遍。考虑到这种异常处理可能源于大脑回路中抑制性和兴奋性驱动的不平衡，我们使用怀孕期间丙戊酸（VPA）诱导的自闭症动物模型来研究初级听觉皮层（AI）的音调组织及其局部抑制回路。我们的结果表明，与对照组相比，VPA 大鼠的初级听觉图发生了扭曲，高频表现过度，感受野广泛调谐，声音强度阈值更高。然而，我们没有检测到 VPA 和对照大鼠 AI 中小白蛋白阳性中间神经元数量的差异。总而言之，我们的研究结果表明，在这种自闭症模型中，听力感知的神经生理学损伤的发生与表达小清蛋白的中间神经元数量的变化无关。这些数据支持这样的观点：精细电路的改变，而不是总体的细胞改变，可能导致自闭症大脑的神经生理学变化。
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.