Objective N-acetyl-5-hydroxytryptamine-methyltransferase (ASMT) is the rate-limiting enzyme for melatonin synthesis and has physiological significance in the regulation of circadian rhythms and mental health.
Methods Male ASMT knockout mice and wild-type mice were randomly divided into sedentary and exercise groups. All were tested for depression behaviorally at the end of the five-week swimming exercise intervention. Anesthetic execution was performed to remove the hippocampal tissue at the end of the behavioral study. Quantitative proteomics techniques were used to detect protein expression in hippocampal tissues and bioinformatics methods were applied for differential protein screening and enrichment pathway analysis.
Results It was found that ASMT knockout mice had a significant depressive-like behavioral phenotype that was significantly improved by swimming exercise intervention. TMT-based quantitative proteomics screened for differential protein functions focused on synaptic signaling pathways, regulation of synaptic chemotransmission, vesicle localization, vesicle-regulated transport at synapses, synaptic vesicle recycling, neurogenesis, regulation of nervous system development, long-term potentiation, and SNARE complex aggregation, etc.
Conclusions The depressive behavior of ASMT knockout mice was associated with abnormal hippocampal synaptic protein expression, which in turn affected the neurotransmitter transmission, synaptic membrane fusion and other functions of hippocampal neurons, and affected synaptic plasticity of hippocampal neurons through signaling pathways such as synaptic vesicle recycling pathway, glutamatergic synaptic pathway, and long-term potentiation. The improvement of depressive-like behaviors in ASMT knockout mice by swimming exercise affects hippocampal neuronal neurogenesis and neuronal differentiation through synaptic vesicle recycling pathway.
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