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可卡因通过 NET 依赖性 PKC 激活增加蓝斑神经元的量子去甲肾上腺素分泌。

Cocaine increases quantal norepinephrine secretion through NET-dependent PKC activation in locus coeruleus neurons.

机构信息

State Key Laboratory of Membrane Biology and Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, College of Future Technology and Peking-Tsinghua Center for Life Sciences and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China.

State Key Laboratory of Membrane Biology and Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, College of Future Technology and Peking-Tsinghua Center for Life Sciences and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China; Core Facilities Center, Departments of Neurobiology and Pathology, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China.

出版信息

Cell Rep. 2022 Aug 16;40(7):111199. doi: 10.1016/j.celrep.2022.111199.

Abstract

The norepinephrine neurons in locus coeruleus (LC-NE neurons) are essential for sleep arousal, pain sensation, and cocaine addiction. According to previous studies, cocaine increases NE overflow (the profile of extracellular NE level in response to stimulation) by blocking the NE reuptake. NE overflow is determined by NE release via exocytosis and reuptake through NE transporter (NET). However, whether cocaine directly affects vesicular NE release has not been directly tested. By recording quantal NE release from LC-NE neurons, we report that cocaine directly increases the frequency of quantal NE release through regulation of NET and downstream protein kinase C (PKC) signaling, and this facilitation of NE release modulates the activity of LC-NE neurons and cocaine-induced stimulant behavior. Thus, these findings expand the repertoire of mechanisms underlying the effects of cocaine on NE (pro-release and anti-reuptake), demonstrate NET as a release enhancer in LC-NE neurons, and provide potential sites for treatment of cocaine addiction.

摘要

蓝斑去甲肾上腺素能神经元(LC-NE 神经元)对于睡眠觉醒、疼痛感知和可卡因成瘾至关重要。根据之前的研究,可卡因通过阻断去甲肾上腺素再摄取来增加去甲肾上腺素溢出(刺激反应中外周去甲肾上腺素水平的特征)。去甲肾上腺素溢出是通过通过胞吐作用释放去甲肾上腺素和通过去甲肾上腺素转运蛋白(NET)再摄取来确定的。然而,可卡因是否直接影响囊泡去甲肾上腺素释放尚未被直接测试。通过记录 LC-NE 神经元的量子去甲肾上腺素释放,我们报告说,可卡因通过调节 NET 和下游蛋白激酶 C(PKC)信号直接增加量子去甲肾上腺素释放的频率,这种去甲肾上腺素释放的促进作用调节 LC-NE 神经元的活动和可卡因诱导的兴奋剂行为。因此,这些发现扩展了可卡因对去甲肾上腺素(前释放和抗再摄取)作用的机制范围,证明 NET 是 LC-NE 神经元中的释放增强剂,并为可卡因成瘾的治疗提供了潜在的靶点。

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