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Enhanced Transient Striatal Dopamine Release and Reuptake in Lphn3 Knockout Rats.
ACS Chemical Neuroscience ( IF 5 ) Pub Date : 2020-03-23 , DOI: 10.1021/acschemneuro.0c00033 Samantha L Regan 1, 2 , Michael T Cryan 3 , Michael T Williams 2 , Charles V Vorhees 2 , Ashley E Ross 1, 3
ACS Chemical Neuroscience ( IF 5 ) Pub Date : 2020-03-23 , DOI: 10.1021/acschemneuro.0c00033 Samantha L Regan 1, 2 , Michael T Cryan 3 , Michael T Williams 2 , Charles V Vorhees 2 , Ashley E Ross 1, 3
Affiliation
Latrophilin-3 (LPHN3) is an adhesion G protein coupled receptor involved in regulating neuroplasticity. Variants of LPHN3 are associated with increased risk of attention-deficit hyperactivity disorder. Data from mouse, zebrafish, Drosophila, and rat show that disruption of LPHN3 results in hyperactivity, and in the Sprague–Dawley Lphn3 knockout rat, exhibit deficits in learning and memory and changes in dopamine (DA) markers in the neostriatum. To determine the effects of Lphn3 deletion on DA neurotransmission, we compared the concentration, duration, and frequency of DA transients in KO and wild-type rats using fast-scan cyclic voltammetry in brain slices. Lphn3 KO rats showed higher release of DA, and the duration and interevent time were markedly decreased compared with wild-type rats. The data demonstrate that LPHN3 plays a heretofore unrecognized role in DA signaling and may represent a new target for small molecule regulation of DA neurotransmission with translational implications.
中文翻译:
Lphn3基因敲除大鼠中增强的瞬时纹状体多巴胺释放和再摄取。
Latrophilin-3(LPHN3)是参与调节神经可塑性的粘附性G蛋白偶联受体。LPHN3的变体与注意力缺陷多动障碍的风险增加有关。来自小鼠,斑马鱼,果蝇和大鼠的数据表明,LPHN3的破坏导致过度活跃,而在Sprague-Dawley Lphn3基因敲除的大鼠中,新纹状体表现出学习和记忆障碍以及多巴胺(DA)标记的变化。为了确定Lphn3缺失对DA神经传递的影响,我们使用快速扫描循环伏安法在脑切片中比较了KO和野生型大鼠中DA瞬变的浓度,持续时间和频率。Lphn3KO大鼠表现出较高的DA释放,并且与野生型大鼠相比,其持续时间和间歇时间明显减少。数据表明,LPHN3在DA信号传导中起迄今未发现的作用,并可能代表小分子调控DA神经传递的新靶标,具有翻译意义。
更新日期:2020-04-23
中文翻译:
Lphn3基因敲除大鼠中增强的瞬时纹状体多巴胺释放和再摄取。
Latrophilin-3(LPHN3)是参与调节神经可塑性的粘附性G蛋白偶联受体。LPHN3的变体与注意力缺陷多动障碍的风险增加有关。来自小鼠,斑马鱼,果蝇和大鼠的数据表明,LPHN3的破坏导致过度活跃,而在Sprague-Dawley Lphn3基因敲除的大鼠中,新纹状体表现出学习和记忆障碍以及多巴胺(DA)标记的变化。为了确定Lphn3缺失对DA神经传递的影响,我们使用快速扫描循环伏安法在脑切片中比较了KO和野生型大鼠中DA瞬变的浓度,持续时间和频率。Lphn3KO大鼠表现出较高的DA释放,并且与野生型大鼠相比,其持续时间和间歇时间明显减少。数据表明,LPHN3在DA信号传导中起迄今未发现的作用,并可能代表小分子调控DA神经传递的新靶标,具有翻译意义。