期刊
NEUROCHEMICAL RESEARCH
卷 -, 期 -, 页码 -出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-023-04056-x
关键词
beta-glucan; Hippocampus; Microglia; Antidepressant
The decline of microglia in the hippocampus has been linked to the development of depression, and the reversal of this decline shows antidepressant effects. Beta-glucan, a polysaccharide, has beneficial effects on the nervous system and may correct the functional deficiency of microglia. In animal studies, beta-glucan administration reversed depression-like behaviors induced by chronic stress and its effects were mediated by microglia stimulation.
In recent years, the decline of microglia in the hippocampus has been shown to play a role in the development of depression, and its reversal shows marked antidepressant-like effects. beta-glucan is a polysaccharide from Saccharomyces cerevisiae and has numerous beneficial effects on the nervous system, including improving axon regeneration and cognition. Considering its immuno-stimulatory activities in cultured microglia and brain tissues, we hypothesize that beta-glucan may be a potential candidate to correct the functional deficiency of microglia and thereby alleviate depression-like behaviors in chronically stressed animals. An expected, our results showed that a single injection of beta-glucan 5 h before behavioral tests at a dose of 10 or 20 mg/kg, but not at a dose of 5 mg/kg, reversed the depression-like behavior induced by chronic stress in mice in the tail suspension test, forced swimming test, and sucrose preference test. The effect of beta-glucan (20 mg/kg) also showed time-dependent properties that were statistically significant 5 and 8, but not 3, hours after drug injection and persisted for at least 7 days. Fourteen days after beta-glucan injection, no antidepressant-like effect was observed anymore. However, this effect was overcome by a second beta-glucan injection (20 mg/kg) 14 days after the first beta-glucan injection. Stimulation of microglia appeared to mediate the antidepressant-like effect of beta-glucan, because both inhibition of microglia and their depletion prevented the antidepressant-like effect of beta-glucan. Based on these effects of beta-glucan, beta-glucan administration could be developed as a new strategy for the treatment of depression.
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