The mechanistic underpinnings of autism remain a subject of debate and controversy. Why do individuals with autism share an overlapping set of atypical behaviors and symptoms, despite having different genetic and environmental risk factors? A major challenge in developing new therapies for autism has been the inability to identify convergent neural phenotypes that could explain the common set of symptoms that result in the diagnosis. Although no striking macroscopic neuropathological changes have been identified in autism, there is growing evidence that inhibitory interneurons (INs) play an important role in its neural basis. In this Review, we evaluate and interpret this evidence, focusing on recent findings showing reduced density and activity of the parvalbumin class of INs. We discuss the need for additional studies that investigate how genes and the environment interact to change the developmental trajectory of INs, permanently altering their numbers, connectivity and circuit engagement.

自闭症的机制基础仍然是争论和争议的主题。尽管具有不同的遗传和环境风险因素，为什么自闭症患者会有一组重叠的非典型行为和症状？开发自闭症新疗法的一个主要挑战是无法识别可以解释导致诊断的常见症状集的会聚神经表型。尽管在自闭症中没有发现显着的宏观神经病理学变化，但越来越多的证据表明抑制性中间神经元 (INs) 在其神经基础中起着重要作用。在这篇综述中，我们评估和解释了这一证据，重点关注最近的发现，这些发现表明小清蛋白类 IN 的密度和活性降低。