Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
Clinical Neuroscience Research Unit, Connecticut Mental Health Center, New Haven, CT, USA.
Mol Psychiatry. 2024 Sep;29(9):2873-2885. doi: 10.1038/s41380-024-02519-3. Epub 2024 Apr 2.
The elucidation of synaptic density changes provides valuable insights into the underlying brain mechanisms of substance use. In preclinical studies, synaptic density markers, like spine density, are altered by substances of abuse (e.g., alcohol, amphetamine, cannabis, cocaine, opioids, nicotine). These changes could be linked to phenomena including behavioral sensitization and drug self-administration in rodents. However, studies have produced heterogeneous results for spine density across substances and brain regions. Identifying patterns will inform translational studies given tools that now exist to measure in vivo synaptic density in humans. We performed a meta-analysis of preclinical studies to identify consistent findings across studies. PubMed, ScienceDirect, Scopus, and EBSCO were searched between September 2022 and September 2023, based on a protocol (PROSPERO: CRD42022354006). We screened 6083 publications and included 70 for meta-analysis. The meta-analysis revealed drug-specific patterns in spine density changes. Hippocampal spine density increased after amphetamine. Amphetamine, cocaine, and nicotine increased spine density in the nucleus accumbens. Alcohol and amphetamine increased, and cannabis reduced, spine density in the prefrontal cortex. There was no convergence of findings for morphine's effects. The effects of cocaine on the prefrontal cortex presented contrasting results compared to human studies, warranting further investigation. Publication bias was small for alcohol or morphine and substantial for the other substances. Heterogeneity was moderate-to-high across all substances. Nonetheless, these findings inform current translational efforts examining spine density in humans with substance use disorders.
阐明突触密度变化提供了有价值的见解,了解物质使用的潜在大脑机制。在临床前研究中,突触密度标志物,如棘密度,被滥用物质改变(例如,酒精、安非他命、大麻、可卡因、阿片类药物、尼古丁)。这些变化可能与现象有关,包括行为敏感化和啮齿动物的药物自我给药。然而,研究在不同物质和大脑区域的棘密度方面产生了不一致的结果。鉴于现在存在测量人类体内突触密度的工具,确定模式将为转化研究提供信息。我们对临床前研究进行了荟萃分析,以确定研究之间的一致发现。根据协议(PROSPERO:CRD42022354006),在 2022 年 9 月至 2023 年 9 月期间,在 PubMed、ScienceDirect、Scopus 和 EBSCO 上进行了搜索。我们筛选了 6083 篇出版物,并纳入了 70 篇进行荟萃分析。荟萃分析显示,棘密度变化存在药物特异性模式。安非他命后海马棘密度增加。安非他命、可卡因和尼古丁增加伏隔核的棘密度。酒精和安非他命增加,大麻减少前额叶皮质的棘密度。吗啡作用的发现没有收敛。可卡因对前额叶皮质的影响与人类研究结果相反,值得进一步研究。酒精或吗啡的发表偏倚较小,而其他物质的发表偏倚较大。所有物质的异质性均为中高度。尽管如此,这些发现为当前检查物质使用障碍患者体内棘密度的转化努力提供了信息。