The Mechanism of the Nucleus Accumbens-Ventral Pallidum Pathway Mediated by Drug Withdrawal-Induced High-Seeking Motivation in Cocaine Addiction
文献类型:期刊论文
| 作者 | Tan, Jiayan1,2; Meng, Yiming1,2 ; Du, Wenjie1,2; Jin, Lingtong1,2; Liang, Jing1,2 ; Shen, Fang1,2
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| 刊名 | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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| 出版日期 | 2024-11-01 |
| 卷号 | 25期号:21页码:17 |
| 关键词 | cocaine drug-seeking motivation withdrawal ventral pallidum nucleus accumbens disinhibition |
| ISSN号 | 1661-6596 |
| DOI | 10.3390/ijms252111612 |
| 通讯作者 | Shen, Fang(shenf@psych.ac.cn) |
| 英文摘要 | The reinforcement of drug-seeking motivation following drug withdrawal is recognized as a significant factor contributing to relapse. The ventral pallidum (VP) plays a crucial role in encoding and translating motivational aspects of reward. However, current research lacks a clear understanding of how the VP mediates drug-seeking motivation and the feedback modulation between the VP and the nucleus accumbens (NAc) following drug withdrawal. Therefore, utilizing a rat model of cocaine self-administration, we investigated the circuitry mechanisms underlying drug-seeking behavior post-drug withdrawal involving the NAc-VP pathway. Initially, we observed a significant enhancement in drug-seeking behavior 14 days after cocaine withdrawal. Subsequently, we identified the feedback mechanism through which the NAc-VP regulates this behavior. Immunofluorescence results indicated an increase in c-Fos expression levels in the ventral pallidum ventromedial (VPvm) and ventrolateral ventral pallidum (VPvl) following drug withdrawal. Calcium fiber photometry further elucidated that during the expression of high motivational drug-seeking behavior, there was a specific enhancement in VPvm neuronal activity, and retrograde tracing techniques suggested a weakened transmission function in the NAc-VPm pathway. Additionally, chemical genetic techniques demonstrated that inhibiting the activity of the NAc-VP pathway could increase the motivational level of drug-seeking behavior. These findings indicate that the reduced inhibitory function of the NAc-VP pathway following prolonged cocaine withdrawal forms the basis for heightened reactivity in VPvm neurons, thus regulating the expression of high motivational behavior triggered by drug-related cues. Our study results suggest that maintaining normal NAc-VP pathway functionality may decrease drug-seeking motivation post long-term drug withdrawal, offering new insights for interventions targeting relapse. |
| 收录类别 | SCI |
| WOS关键词 | DECISION-MAKING ; TEGMENTAL AREA ; NEURONS ; INCUBATION ; PROMOTE ; ROLES |
| 资助项目 | National Natural Science Foundation of China ; CAS Key Laboratory of Mental Health, Institute of Psychology ; [32271137] |
| WOS研究方向 | Biochemistry & Molecular Biology ; Chemistry |
| 语种 | 英语 |
| WOS记录号 | WOS:001351357400001 |
| 出版者 | MDPI |
| 资助机构 | National Natural Science Foundation of China ; CAS Key Laboratory of Mental Health, Institute of Psychology |
| 源URL | [http://ir.psych.ac.cn/handle/311026/49273] ![]() |
| 专题 | 心理研究所_中国科学院心理健康重点实验室 |
| 通讯作者 | Shen, Fang |
| 作者单位 | 1.Univ Chinese Acad Sci, Dept Psychol, Beijing 100101, Peoples R China 2.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, 16 Lin Cui Rd, Beijing 100101, Peoples R China |
| 推荐引用方式 GB/T 7714 | Tan, Jiayan,Meng, Yiming,Du, Wenjie,et al. The Mechanism of the Nucleus Accumbens-Ventral Pallidum Pathway Mediated by Drug Withdrawal-Induced High-Seeking Motivation in Cocaine Addiction[J]. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES,2024,25(21):17. |
| APA | Tan, Jiayan,Meng, Yiming,Du, Wenjie,Jin, Lingtong,Liang, Jing,&Shen, Fang.(2024).The Mechanism of the Nucleus Accumbens-Ventral Pallidum Pathway Mediated by Drug Withdrawal-Induced High-Seeking Motivation in Cocaine Addiction.INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES,25(21),17. |
| MLA | Tan, Jiayan,et al."The Mechanism of the Nucleus Accumbens-Ventral Pallidum Pathway Mediated by Drug Withdrawal-Induced High-Seeking Motivation in Cocaine Addiction".INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 25.21(2024):17. |
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来源:心理研究所
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