Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas y Universidad Miguel Hernández, 03550 Sant Joan d'Alacant, Spain.
Nat Rev Neurosci. 2012 Jan 18;13(2):107-20. doi: 10.1038/nrn3155.
Schizophrenia, autism and intellectual disabilities are best understood as spectrums of diseases that have broad sets of causes. However, it is becoming evident that these conditions also have overlapping phenotypes and genetics, which is suggestive of common deficits. In this context, the idea that the disruption of inhibitory circuits might be responsible for some of the clinical features of these disorders is gaining support. Recent studies in animal models demonstrate that the molecular basis of such disruption is linked to specific defects in the development and function of interneurons - the cells that are responsible for establishing inhibitory circuits in the brain. These insights are leading to a better understanding of the causes of schizophrenia, autism and intellectual disabilities, and may contribute to the development of more-effective therapeutic interventions.
精神分裂症、自闭症和智力障碍最好被理解为具有广泛病因的疾病谱。然而，这些病症具有重叠的表型和遗传学，这表明它们存在共同的缺陷，这一点变得越来越明显。在这种情况下，抑制回路的中断可能是这些疾病的一些临床特征的原因的观点正在得到支持。动物模型的最新研究表明，这种中断的分子基础与中间神经元发育和功能的特定缺陷有关，中间神经元是大脑中负责建立抑制回路的细胞。这些新见解使我们对精神分裂症、自闭症和智力障碍的病因有了更好的理解，并可能有助于开发更有效的治疗干预措施。
