Abstract
[Purpose]Chronic stress affects the neuronal architecture of hippocampal subfields including the Cornu Ammonis 1 (CA1) region, which governs long-term memory. Exercise exerts a beneficial effect on memory improvement via hippocampal AMP-activated protein kinase (AMPK) activation. However, the relationship between the two phenomena is poorly understood. This study used animal and cell culture experimental systems to investigate whether chronic stress-induced impairment of memory consolidation and maladaptation of the neuronal architecture in the hippocampal CA1 area is prevented by regular exercise through AMPK activation.[Methods]Mice underwent four weeks of treadmill running with or without a 6h/21d-restraint stress regimen, along with treatment with Compound C. Memory consolidation was assessed using the Morris Water Maze (MWM). Dendritic rearrangement of hippocampal CA1 neurons was evaluated using the Golgi-Cox stain and Sholl analysis. Additionally, the primary hippocampal culture system was adopted for in vitro experiments.[Results]Chronic stress-induced failure of memory retention and reduction in AMPK activation were ameliorated by the exercise regimen. Chronic stress-or repeated corticosterone (CORT)-provoked malformation of the neuronal architecture was also suppressed by both exercise and treatment with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR).[Conclusion]Chronic stress causes dendritic retraction among dorsal hippocampal CA1 neurons via the downregulation of AMPK activation, thereby leading to failure of memory retention. In contrast, regular exercise protects against chronic stress-evoked defects in memory consolidation and changes in neuronal morphology in the dorsal hippocampal CA1 area via mild activation of AMPK.
Highlights
Chronic stress is a risk factor for cognitive- and/or mood-related behavioral abnormalities that are involved in abnormal synaptic plasticity in the dorsal hippocampus[1,2].A large body of evidence has demonstrated that chronic stress alters structural and functional plasticity in some limbic structures such as the prefrontal cortex (PFC), hippocampus, and amygdala[3,4,5,6]
The current study demonstrated that chronic stress caused memory consolidation failure and reduced AMPK activity in the hippocampal Cornu Ammonis 1 (CA1) region, which was prevented by regular exercise
We found that regular exercise rescues chronic stress-induced failure of long-term memory and downregulation of AMPK activity
Summary
Chronic stress is a risk factor for cognitive- and/or mood-related behavioral abnormalities that are involved in abnormal synaptic plasticity in the dorsal hippocampus[1,2].A large body of evidence has demonstrated that chronic stress alters structural and functional plasticity in some limbic structures such as the prefrontal cortex (PFC), hippocampus, and amygdala[3,4,5,6]. Chronic stress is a risk factor for cognitive- and/or mood-related behavioral abnormalities that are involved in abnormal synaptic plasticity in the dorsal hippocampus[1,2]. Chronic stress-induced morphological and molecular alterations in PFC neurons are similar to those reported in the hippocampus[7,8,9], suggesting that chronic stress results in aberrant structural plasticity such as dendritic shrinkage in the PFC and hippocampus, which leads to impaired cognitive-related behaviors. Some studies suggest that chronic stress-induced decline in synaptic efficacy among hippocampal CA1 neurons may be responsible for the observed abnormal structural plasticity. This leads to long-term memory consolidation failure[11,12,13]. One conceivable mechanism underlying hippocampus-dependent memory persistence is the structural plasticity of dendrites, which is a key component in determining synaptic properties such as synaptic efficacy and excitatory neurotransmission
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