The potential role of exercise in chronic stress-related changes in AMPA receptor phenotype underlying synaptic plasticity.

Abstract

[Purpose] 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. [Methods] The present article reviews the information about the chronic stress-related synaptic plasticity and the role of exercise from the previous-published articles. [Results] 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. [Conclusion] The present article discusses the relationship between AMPARs and synaptic plasticity in chronic stress, as well as the potential role of exercise.