【摘 要】
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Growing evidence has implicated glial anomalies in the pathophysiology of major depression disorder (MDD).Gap junctional communication is a main determinant of astrocytic function.However, it is uncle
【机 构】
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Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences & Pekin
【出 处】
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第十五届中国神经精神药理学学术会议
论文部分内容阅读
Growing evidence has implicated glial anomalies in the pathophysiology of major depression disorder (MDD).Gap junctional communication is a main determinant of astrocytic function.However, it is unclear whether gap junction dysfunc tion is involved in MDD development.This study investigates changes in the function of astrocyte gap junction occurring in the rat prefrontal cortex (PFC) after chronic unpredictable stress (CUS), a rodent model of depression.Animals exposed to CUS and showing behavioral deficits in sucrose preference test (SPT)and novelty suppressed feeding test (NSFT) exhibited significant decreases in diffusion of gap junction channel-permeable dye and expression of connexin 43 (Cx43), a major component of astro cyte gap junction, and abnormal gap junctional ultrastructure in the PFC.Furthermore, we analyzed the effects of typical antide pressants fluoxetine and duloxetine and glucocorticoid receptor (GR) antagonist mifepristone on CUS-induced gap junctional dysfunction and depressive-like behaviors.The cellular and be havioral alterations induced by CUS were reversed and/or blocked by treatment with typical antidepressants or mifepris tone, indicating the mechanism of their antidepressant action may involve the amelioration of gap junction dysfunction and the the cellular changes may be related to GR activation.
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