Leem Yea-Hyun
J Exerc Nutrition Biochem. 2017 Dec 31;21(4):11-15. doi: 10.20463/jenb.2017.0037.
Chronic stress can cause disturbances in synaptic plasticity, such as longterm potentiation, along with behavioral defects including memory deficits. One major mechanism sustaining synaptic plasticity involves the dynamics and contents of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in the central nervous system. In particular, chronic stress-induced disruption of AMPARs includes it abnormal expression, trafficking, and calcium conductance at glutamatergic synapses, which contributes to synaptic plasticity at excitatory synapses. Exercise has the effect of promoting synaptic plasticity in neurons. However, the contribution of exercise to AMPAR behavior under chronic stressful maladaptation remains unclear.
The present article reviews the information about the chronic stress-related synaptic plasticity and the role of exercise from the previous-published articles.
AMPAR-mediated synaptic transmission is an important for chronic stress-related changes of synaptic plasticity, and exercise may at least partly contribute to these episodes.
The present article discusses the relationship between AMPARs and synaptic plasticity in chronic stress, as well as the potential role of exercise.
慢性应激可导致突触可塑性紊乱，如长时程增强，同时伴有包括记忆缺陷在内的行为缺陷。维持突触可塑性的一个主要机制涉及中枢神经系统中α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPARs）的动态变化和含量。特别是，慢性应激诱导的AMPARs破坏包括其在谷氨酸能突触处的异常表达、转运和钙电导，这有助于兴奋性突触的突触可塑性。运动具有促进神经元突触可塑性的作用。然而，在慢性应激适应不良的情况下，运动对AMPAR行为的影响仍不清楚。
本文回顾了以往发表的关于慢性应激相关突触可塑性和运动作用的信息。
AMPAR介导的突触传递对于慢性应激相关的突触可塑性变化很重要，运动可能至少部分促成了这些过程。
本文讨论了慢性应激中AMPARs与突触可塑性之间的关系，以及运动的潜在作用。
