期刊
NEURON
卷 109, 期 13, 页码 2165-+出版社
CELL PRESS
DOI: 10.1016/j.neuron.2021.05.002
关键词
-
资金
- NIH [R01MH108594, R01DA049787, U01MH114829]
- Canadian Institutes of Health Research (CIHR) postdoctoral fellowship
- TobaccoRelated Disease ResearchProgram (TRDRP) postdoctoral fellowship
- NIH T32 training grant
- American Heart Association predoctoral fellowship
This study demonstrates how dopamine receptor D3 (DRD3)-dependent plasticity in the ventral pallidum (VP) drives potentiation of dopamine release in the nucleus accumbens to facilitate relapse to cocaine seeking. Understanding circuit-specific DRD3-mediated plasticity contributes to the process of drug relapse.
Drugs of abuse induce persistent remodeling of reward circuit function, a process thought to underlie the emergence of drug craving and relapse to drug use. However, how circuit-specific, drug-induced molecular and cellular plasticity can have distributed effects on the mesolimbic dopamine reward system to facilitate relapse to drug use is not fully elucidated. Here, we demonstrate that dopamine receptor D3 (DRD3)-dependent plasticity in the ventral pallidum (VP) drives potentiation of dopamine release in the nucleus accumbens during relapse to cocaine seeking after abstinence. We show that two distinct VP DRD3(+) neuronal populations projecting to either the lateral habenula (LHb) or the ventral tegmental area (VTA) display different patterns of activity during drug seeking following abstinence from cocaine self-administration and that selective suppression of elevated activity or DRD3 signaling in the LHb-projecting population reduces drug seeking. Together, our results uncover how circuit-specific DRD3-mediated plasticity contributes to the process of drug relapse.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据