【摘 要】
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It is well-established that neuroimmunity is involved in the pathophysiology and treatment of mood disorders.Dectin-1 is a β-glucan(including lentinan; LNT)receptor that regulates immune functions and
【机 构】
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State Key Laboratory for Conservation and Utilization of Bio-resources in Yunnan,Yunnan University,K
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
It is well-established that neuroimmunity is involved in the pathophysiology and treatment of mood disorders.Dectin-1 is a β-glucan(including lentinan; LNT)receptor that regulates immune functions and cytokine expression in many immune cell types.Cumulative evidence has suggested that the glutamatergic system seems to play an important role in the treatment of depression.Here,we identified Dectin-1 as the β-glucan receptor that mediates the antidepressant effects of LNT by regulating the functions of AMPA receptors.We found that treatment with LNT for 60 minutes leads to a significant antidepressant effect in the tail suspension test(TST)and the forced swim test(FST)in mice.After 1 day or 5 days of injections with LNT,the antidepressant effects of LNT in TST and FST remained.Additionally,LNT did not show a hyperactive effect in the open field test.Dectin-1 receptor levels were increased after LNT treatment for 5 days and the specific Dectin-1 inhibitor laminarin was able to block the antidepressant effect of LNT.After 5 days of treatment,LNT enhanced anti-inflammatory cytokine interleukin-4(IL-4),without affecting inflammatory cytokines tumor necrosis factor-alpha(TNF-α)and interleukin-1β(IL-1β),and also enhanced p-GluR1(S845)in the prefrontal cortex(PFC); however,the total GluR1,GluR2,and GluR3 expression levels remained unchanged.We also found that the AMPA-specific blocker GYKI 52466 was able to block the antidepressant effect of LNT.This study identified Dectin-1 as a novel target for the antidepressant drug development and determined its beneficial mechanism in regulating the glutamate receptor signaling pathway.
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