核 accumbens 贝神经元对可卡因的早期敏感性与未来药物摄入量增加有关
Ashley K Crawley1,2, Anirudh Sharma1,3, Kevin R Coffey4
1Department of Psychology, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Addiction neuroscience
|September 4, 2023
概括
早期暴露于可卡因会改变核聚集体 (NAc) 神经元的敏感性,从而预测未来的药物摄入量. 这种NAc外神经元的敏感性与可卡因自我管理的增加相关,为成敏感性查和治疗提供了潜在的标.
科学领域:
- 神经科学是一个神经科学.
- 成研究 研究成研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 药物使用障碍涉及条纹体,慢性可卡因使用会改变多巴胺和神经元发射.
- 早期药物反应的个体差异显著影响成易感受性.
研究的目的:
- 为了研究慢性可卡因自我管理 (SA) 期间背部和腹部条状神经元激发的变化.
- 为了确定早期药物暴露后条纹发射的个体差异是否与增加的药物摄入有关.
主要方法:
- 使用现有数据进行纵向药理动力学建模.
- 在老鼠的慢性可卡因S-A期间,对核 (NAc) 核心和外中神经元发射模式的分析.
主要成果:
- 在最初的6个SA会话中,NAc核心和外神经元对可卡因的敏感性增加.
- 在慢性SA期间,药物摄入量和神经元发射率之间存在负相关性.
- 早期可卡因诱导的NAc外神经元抑制预测了未来可卡因摄入量的增加.
结论:
- 在NAc外中对可卡因的早期神经元敏感性与增加的成易感性有关.
- 识别与这种敏感性相关的遗传或可用药物标可以使早期查成风险成为可能.
- 这一发现可能会导致对物质使用障碍的新型预防性药物疗法.
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