[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.
The potential role of exercise in chronic stress-related changes in AMPA receptor phenotype underlying synaptic plasticity
Published 2017 in The Journal of Exercise Nutrition and Biochemistry
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
The Journal of Exercise Nutrition and Biochemistry
- Publication date
2017-12-31
- Fields of study
Biology, Medicine, Environmental Science
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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