Alteration in NMDAR subunits in different brain regions of chronic unpredictable mild stress (CUMS) rat model.

IF 2.2 4区 医学 Q4 NEUROSCIENCES Translational Neuroscience Pub Date : 2022-10-26 eCollection Date: 2022-01-01 DOI:10.1515/tnsci-2022-0255
Jing Chen, Yanmin Luo, Xin Liang, Xiangru Kong, Qian Xiao, Jing Tang, Yingqiang Qi, Yong Tang, Yun Xiu
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引用次数: 1

Abstract

N-Methyl-d-aspartate receptor (NMDAR) signaling pathway has been implicated in the pathogenesis and treatment of depression. However, the role of NMDAR subunits in depression is still unclear. In this study, alteration in all seven NMDAR subunits in several brain areas of rats exposed to chronic unpredictable mild stress (CUMS), an animal model of depression, was detected. Our findings demonstrated that: (1) CUMS could induce a reduction in sucrose preference, an indicator of typical depression-like behaviors; (2) CUMS significantly reduced the NMDAR subunits of GluN2B and GluN3 in the medial prefrontal cortex (mPFC), but not altered all seven NMDAR subunits in hippocampus and corpus callosum of rats; (3) subunit composition of NMDARs in corpus callosum was different from that in mPFC, PFC and hippocampus; and (4) the mRNA expressions of GluN2B, GluN3A and GluN3B in mPFC as well as mRNA expression of GluN2C in corpus callosum were correlated to sucrose preference in rats. These findings suggested that GluN2B and GluN3 in mPFC may contribute to the pathophysiology of depression.

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慢性不可预测轻度应激(CUMS)大鼠模型不同脑区NMDAR亚基的改变。
n -甲基-d-天冬氨酸受体(NMDAR)信号通路与抑郁症的发病和治疗有关。然而,NMDAR亚基在抑郁症中的作用尚不清楚。在这项研究中,在暴露于慢性不可预测的轻度应激(CUMS)的大鼠的几个脑区域中,检测到所有七个NMDAR亚基的改变,这是一种抑郁症的动物模型。研究结果表明:(1)CUMS可诱导典型抑郁样行为的蔗糖偏好降低;(2) CUMS显著降低了大鼠内侧前额叶皮层(mPFC)中GluN2B和GluN3的NMDAR亚基,但未改变海马和胼胝体中所有7个NMDAR亚基;(3)胼胝体中NMDARs的亚基组成不同于mPFC、PFC和海马;(4)大鼠mPFC中GluN2B、GluN3A和GluN3B的mRNA表达以及胼胝体中GluN2C的mRNA表达与蔗糖偏好相关。这些发现提示mPFC中GluN2B和GluN3可能参与抑郁症的病理生理。
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来源期刊
CiteScore
3.00
自引率
4.80%
发文量
45
审稿时长
>12 weeks
期刊介绍: Translational Neuroscience provides a closer interaction between basic and clinical neuroscientists to expand understanding of brain structure, function and disease, and translate this knowledge into clinical applications and novel therapies of nervous system disorders.
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