Reverte Ingrid, Marchetti Claudia, Pezza Sara, Zenoni Soami F, Scaringi Giorgia, Ferrucci Laura, D'Ottavio Ginevra, Pignataro Annabella, Andolina Diego, Raspa Marcello, Scavizzi Ferdinando, Venniro Marco, Ramsey Leslie A, Gross Cornelius, Caprioli Daniele, Ragozzino Davide
Department of Physiology and Pharmacology, Sapienza University, Laboratory affiliated to Institute Pasteur Italia - Fondazione Cenci Bolognetti, Rome, Italy; IRCCS Santa Lucia Foundation, Rome, Italy.
IRCCS Santa Lucia Foundation, Rome, Italy; Institute of Translational Pharmacology, National Research Council, CNR, Rome, Italy.
Brain Behav Immun. 2024 Jan;115:535-542. doi: 10.1016/j.bbi.2023.11.007. Epub 2023 Nov 13.
During withdrawal from cocaine, calcium permeable-AMPA receptors (CP-AMPAR) progressively accumulate in nucleus accumbens (NAc) synapses, a phenomenon linked to behavioral sensitization and drug-seeking. Recently, it has been suggested that neuroimmune alterations might promote aberrant changes in synaptic plasticity, thus contributing to substance abuse-related behaviors. Here, we investigated the role of microglia in NAc neuroadaptations after withdrawal from cocaine-induced conditioned place preference (CPP). We depleted microglia using PLX5622-supplemented diet during cocaine withdrawal, and after the place preference test, we measured dendritic spine density and the presence of CP-AMPAR in the NAc shell. Microglia depletion prevented cocaine-induced changes in dendritic spines and CP-AMPAR accumulation. Furthermore, microglia depletion prevented conditioned hyperlocomotion without affecting drug-context associative memory. Microglia displayed fewer number of branches, resulting in a reduced arborization area and microglia control domain at late withdrawal. Our results suggest that microglia are necessary for the synaptic adaptations in NAc synapses during cocaine withdrawal and therefore represent a promising therapeutic target for relapse prevention.
在从可卡因戒断期间,钙通透性 - AMPA 受体(CP - AMPAR)在伏隔核(NAc)突触中逐渐积累,这一现象与行为敏化和觅药行为有关。最近,有人提出神经免疫改变可能会促进突触可塑性的异常变化,从而导致与药物滥用相关的行为。在此,我们研究了小胶质细胞在可卡因诱导的条件性位置偏爱(CPP)戒断后 NAc 神经适应性中的作用。在可卡因戒断期间,我们使用添加 PLX5622 的饮食耗尽小胶质细胞,在位置偏爱测试后,我们测量了 NAc 壳中的树突棘密度和 CP - AMPAR 的存在情况。小胶质细胞耗竭可防止可卡因诱导的树突棘变化和 CP - AMPAR 积累。此外,小胶质细胞耗竭可防止条件性活动亢进,而不影响药物 - 环境联想记忆。在戒断后期,小胶质细胞的分支数量减少,导致分支区域和小胶质细胞控制域减小。我们的结果表明,小胶质细胞对于可卡因戒断期间 NAc 突触的突触适应性是必需的,因此代表了预防复发的一个有前景的治疗靶点。