Insel T R, O'Brien D J, Leckman J F
Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia 30322, USA.
Biol Psychiatry. 1999 Jan 15;45(2):145-57. doi: 10.1016/s0006-3223(98)00142-5.
Autism is a poorly understood developmental disorder characterized by social impairment, communication deficits, and compulsive behavior. The authors review evidence from animal studies demonstrating that the nonapeptides, oxytocin and vasopressin, have unique effects on the normal expression of species-typical social behavior, communication, and rituals. Based on this evidence, they hypothesize that an abnormality in oxytocin or vasopressin neurotransmission may account for several features of autism. As autism appears to be a genetic disorder, mutations in the various peptide, peptide receptor, or lineage-specific developmental genes could lead to altered oxytocin or vasopressin neurotransmission. Many of these genes have been cloned and sequenced, and several polymorphisms have been identified. Recent gene targeting studies that alter expression of either the peptides or their receptors in the rodent brain partially support the autism hypothesis. While previous experience suggests caution in hypothesizing a cause or suggesting a treatment for autism, the available preclinical evidence with oxytocin and vasopressin recommends the need for clinical studies using gene scanning, pharmacological and neurobiological approaches.
自闭症是一种了解甚少的发育障碍,其特征为社交障碍、沟通缺陷和强迫行为。作者回顾了来自动物研究的证据,这些证据表明九肽、催产素和加压素对物种典型社交行为、沟通及仪式的正常表达具有独特影响。基于这些证据,他们推测催产素或加压素神经传递异常可能是自闭症的若干特征的原因。由于自闭症似乎是一种遗传性疾病,各种肽、肽受体或谱系特异性发育基因的突变可能导致催产素或加压素神经传递改变。其中许多基因已被克隆和测序,并且已鉴定出几种多态性。最近在啮齿动物大脑中改变肽或其受体表达的基因靶向研究部分支持了自闭症假说。虽然以往经验表明在对自闭症的病因进行假设或提出治疗方法时需谨慎,但目前关于催产素和加压素的临床前证据表明有必要采用基因扫描、药理学和神经生物学方法进行临床研究。