锌在孤独症谱系障碍中调控谷氨酸能受体的研究新进展OA

Autism spectrum disorder(ASD)is a neurodevelopmental disorder characterized by deficits in social communication and repetitive behaviors and interests,with a complex pathogenesis including neuroinflammation,metabolic disturbance of zinc and abnormal neurotransmission.Prenatal zinc deficiency can increase the incidence of ASD in the offspring.On the contrary,prenatal zinc supplementation can significantly reduce the incidence of ASD in the offspring.Glutamate is a major mediator of excitatory synaptic transmission.Abnormal glutamatergic neurotransmission can exacerbate pathological changes in ASD.This process primarily involves ionotropic glutamate receptors,on which the dynamic balance of zinc-regulated excitatory and inhibitory synaptic neurotransmission also depends.However,the role and potential mechanisms of zinc in post-ASD glutamatergic neurotransmission remain to be explored.In this paper,the physiological function of zinc,glutaminergic synaptic signal transduction,and the potential mechanism of zinc regulation of glutaminergic receptors after ASD were reviewed in order to explore the potential molecular targets of zinc therapy in patients with ASD.