Brida Kasey L, Day Jeremy J
Department of Neurobiology, University of Alabama at Birmingham, 1825 University Blvd, SHEL 910, Birmingham, AL 35294, USA.
Department of Neurobiology, University of Alabama at Birmingham, 1825 University Blvd, SHEL 910, Birmingham, AL 35294, USA.
Curr Opin Neurobiol. 2025 Apr 30;93:103032. doi: 10.1016/j.conb.2025.103032.
Drugs of abuse result in well-characterized changes in synapse function and number in brain reward regions such as the nucleus accumbens. However, recent reports demonstrate that only a small fraction of neurons in the nucleus accumbens are activated in response to psychostimulants such as cocaine. While these "ensemble" neurons are marked by drug-related transcriptional changes in immediate early genes, the mechanisms that ultimately link these early changes to enduring molecular alterations in the same neurons are less clear. In this review, we 1) describe potential mechanisms underlying regulation of diverse plasticity-related gene programs across drug-activated ensembles, 2) discuss factors conferring ensemble recruitment bias within seemingly homogeneous populations, and 3) speculate on the role of chromatin and epigenetic modifiers in gating metaplastic state transitions that contribute to addiction.
滥用药物会导致大脑奖赏区域(如伏隔核)的突触功能和数量发生特征明确的变化。然而,最近的报告表明,在伏隔核中,只有一小部分神经元会对可卡因等精神兴奋剂产生反应而被激活。虽然这些“整体”神经元以即时早期基因中与药物相关的转录变化为特征,但将这些早期变化最终与同一神经元中持久的分子改变联系起来的机制尚不清楚。在这篇综述中,我们:1)描述药物激活的神经元群体中各种可塑性相关基因程序调控的潜在机制;2)讨论在看似同质的群体中赋予整体募集偏向性的因素;3)推测染色质和表观遗传修饰因子在促成成瘾的元可塑性状态转变中的作用。