More and more evidences support that the abnormality of GABAergic interneurons is associated with autism spectrum disorders (ASD), epilepsy, schizophrenia and other neurodevelopmental disorders. In recent years, numerous drugs have been developed to regulate ion channels and receptors in GABAergic interneurons, including sodium channels and N-methyl-D-aspartate (NMDA) receptors. The activators of Na+ channel can enhance the action potential of GABAergic interneurons by reducing the inactivation of Na+ channel. NMDA receptor, as a potential therapeutic target of ASD, can restore the NMDA function of GABAergic interneurons, which would be used to treat behavioral defects. In addition, there are many ion channels and receptors on GABAergic interneurons related to ASD. This article reviews GABAergic interneurons in the pathogenesis of ASD and the related interventions.
越来越多的研究证据支持γ-氨基丁酸能中间神经元异常与自闭症谱系障碍（ASD）、癫痫以及精神分裂症等神经发育类疾病有关。近年来研究发现多种药物能靶向调控γ-氨基丁酸能中间神经元上的离子通道及受体，其中主要是钠离子通道和N-甲基-D-天冬氨酸（NMDA）受体等。钠离子通道的激活剂通过降低钠离子通道的失活来增强γ-氨基丁酸能中间神经元的动作电位；NMDA受体作为ASD的潜在治疗靶点，可以通过药物恢复γ-氨基丁酸能中间神经元的NMDA功能来治疗行为学缺陷。此外，γ-氨基丁酸能中间神经元上还有多种离子通道及受体均与ASD有关，未来会有更多药物应用于对γ-氨基丁酸能中间神经元的治疗中。本文回顾和讨论了γ-氨基丁酸能中间神经元在ASD发病过程中的作用和机制并据此进行干预的相关研究进展。
Keywords: Autism spectrum disorders; Cortex; GABAergic neurons; Ion channels; Receptors.