Preventing cocaine rooted neuroplasticity

预防可卡因根源的神经可塑性

• 批准号: 7072704
• 负责人: MARGARET M MORAN-SANTA MARIA
• 金额: $ 0.79万
• 依托单位: MEDICAL UNIVERSITY OF SOUTH CAROLINA
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-05-01 至 2006-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7072704
• 关键词: brain electrical activity; cocaine; cystine; drug addiction; drug withdrawal; electrophysiology; glutamate receptor; glutamates; laboratory rat; neural plasticity; neuropharmacology; neurophysiology; nucleus accumbens; predoctoral investigator; prefrontal lobe /cortex; self medication

DESCRIPTION (provided by applicant): The primary goal of the application is to examine changes in synaptic activity that occur during withdrawal and following cocaine primed reinstatement, and seeks to provide further insight into molecular and cellular alterations that underlie addiction. The studies outlined within the application will use electrophysiology to examine our hypotheses. Specifically, Aim 1 will characterize the physiological response of populations of neurons in the nucleus accumbens to prefrontal cortical stimulation. The goal of Aim 2 is to determine the role of cystine/glutamate exchange and group II metabotropic glutamate receptors in mediating synaptic transmission during withdrawal and following a cocaine priming injection. Rats will be trained to self administer cocaine and undergo a 14-21 day withdrawal period. A different group of rats will act yoked saline controls. At the end of the withdrawal period, mPFC glutamatergic efferents will be stimulated and field recordings measured in the core of the nucleus accumbens.

描述（由申请人提供）： 该应用程序的主要目标是检查在戒断期间和可卡因引发恢复后发生的突触活动的变化，并寻求进一步了解成瘾的分子和细胞变化。申请中概述的研究将使用电生理学来检验我们的假设。具体而言，目标1将表征前额叶皮质刺激的丘脑核神经元群体的生理反应。目的2的目标是确定胱氨酸/谷氨酸交换和II组代谢型谷氨酸受体介导的突触传递在戒断过程中和可卡因引发注射后的作用。大鼠将接受自我注射可卡因的训练，并经历14-21天的戒断期。另一组大鼠将作为对照组。在停药期结束时，将刺激mPFC交感神经能传出神经，并在延髓核的核心中测量场记录。