Abnormal response to stress and impaired NPS-induced hyperlocomotion, anxiolytic effect and corticosterone increase in mice lacking NPSR1.
Abnormal response to stress and impaired NPS-induced hyperlocomotion, anxiolytic effect and corticosterone increase in mice lacking NPSR1.
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DOI：
10.1016/j.psyneuen.2010.01.012
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发表时间：
2010-09
影响因子：
3.7
通讯作者：
Rothenberg, Marc E.
中科院分区：
文献类型：
--
作者：
Zhu, Hongyan;Mingler, Melissa K.;McBride, Melissa L.;Murphy, Andrew J.;Valenzuela, David M.;Yancopoulos, George D.;Williams, Michael T.;Vorhees, Charles V.;Rothenberg, Marc E.
关键词：
NPSR 1是一种G蛋白偶联受体，在参与应激调节的多个脑区中表达。中枢给予NPSR 1的假定内源性配体NPSR 1，可以诱导过度运动、抗焦虑作用和HPA轴的激活。NPSR 1在大脑中的作用仍然不确定。在这里，我们使用NPSR 1基因靶向小鼠来定义NPSR 1在基础条件下对运动、焦虑和/或抑郁样行为、皮质酮水平、前脉冲抑制声惊吓、学习和记忆以及在NPS诱导的运动激活、抗焦虑和皮质酮释放的功能作用。NPSR 1基因缺陷的雄性小鼠在强迫游泳试验中表现出增强的抑郁样行为，减少的声惊吓反应，以及Morris水迷宫中的微小变化。无论是男性还是女性NPSR 1缺陷小鼠显示基线运动，焦虑样行为，或皮质酮释放后，暴露于强迫游泳试验或甲基苯丙胺的挑战在开放领域的改变。脑室内（ICV）给药后，NPSR 1缺陷型小鼠与WT NPS治疗的小鼠相比，未能显示出正常的NPS诱导的运动、抗焦虑或皮质酮释放增加。这些发现表明，NPSR 1是必不可少的介导行为的影响。
NPSR1 is a G protein coupled receptor expressed in multiple brain regions involved in modulation of stress. Central administration of NPS, the putative endogenous ligand of NPSR1, can induce hyperlocomotion, anxiolytic effects and activation of the HPA axis. The role of NPSR1 in the brain remains unsettled. Here we used NPSR1 gene-targeted mice to define the functional role of NPSR1 under basal conditions on locomotion, anxiety- and/or depression-like behavior, corticosterone levels, acoustic startle with prepulse inhibition, learning and memory, and under NPS-induced locomotor activation, anxiolysis, and corticosterone release. Male, but not female, NPSR1-deficient mice exhibited enhanced depression-like behavior in a forced swim test, reduced acoustic startle response, and minor changes in the Morris water maze. Neither male nor female NPSR1-deficient mice showed alterations of baseline locomotion, anxiety-like behavior, or corticosterone release after exposure to a forced swim test or methamphetamine challenge in an open-field. After intracerebroventricular (ICV) administration of NPS, NPSR1-deficient mice failed to show normal NPS-induced increases in locomotion, anxiolysis, or corticosterone release compared with WT NPS-treated mice. These findings demonstrate that NPSR1 is essential in mediating NPS effects on behavior.
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影响因子：
3.4
作者：
Lucki, I;Dalvi, A;Mayorga, AJ
通讯作者：
Mayorga, AJ
影响因子：
3.4
作者：
Leonard, Sarah K.;Dwyer, Jason M.;Ring, Robert H.
通讯作者：
Ring, Robert H.
影响因子：
3.5
作者：
Maei HR;Zaslavsky K;Teixeira CM;Frankland PW
通讯作者：
Frankland PW
DOI：
10.1124/jpet.108.143867
发表时间：
2009-02
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Camarda V;Rizzi A;Ruzza C;Zucchini S;Marzola G;Marzola E;Guerrini R;Salvadori S;Reinscheid RK;Regoli D;Calò G
通讯作者：
Calò G
影响因子：
4.8
作者：
Müller, MB;Landgraf, R;Wurst, W
通讯作者：
Wurst, W