Abstract
In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the somatic, cognitive, and psychiatric symptoms of depression commonly observed after myocardial infarction. Peripheral 5-hydroxytryptamine is an important substance in the gut-brain axis, and its abnormal metabolism is a critical finding after myocardial infarct.
Highlights
Depression is a common psychiatric symptom of myocardial infarction [1] and is an independent risk factor for disease prognosis
Myocardial infarction has been previously reported to have an effect on intestinal barrier integrity [2] and somatic psychiatric symptoms that reflect the prognosis of the disease
Our experimental findings indicate that the inverse relationship between the level of 5-HT in peripheral blood and the level of 5-HT in the hippocampus is related to high metabolism of 5-HT in the intestine S1 Supporting Information. 5-HT in peripheral blood serves as a bridge between the gut and the brain and is an important regulator of the gut-brain and brain-gut axes
Summary
Depression is a common psychiatric symptom of myocardial infarction [1] and is an independent risk factor for disease prognosis. Low metabolism of hippocampal 5-HT leads to abnormalities in brain regions associated with learning, memory, and emotion It functions through the binding of its receptors, including the G-protein coupled 5-HT1A receptor, which is a predominant contributor to the regulation of emotion in the hippocampal CA1 region and the dentate gyrus. Animal studies have shown that the levels and metabolism of 5-HT in the hippocampus are low in rats with post-infectious irritable bowel syndrome [5]. These data suggest that the hippocampus is involved in the regulation of gastrointestinal function
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