美国约翰霍普金斯大学Gül Dölen研究组经过不懈努力而取得。相关论文于2023年6月14日发表在《自然》杂志上。

研究人员在小鼠身上证明了重新开启社会奖励学习关键期的能力是各种迷幻药的共同特性。值得注意的是，关键期重开的时间过程与人类报告的急性主观效应的持续时间成正比。此外，在成年后恢复社会奖励学习的能力与催产素介导的伏隔核长期抑制的变态恢复相一致。最后，在“开放状态”与“封闭状态”下不同表达基因的鉴定提供了证据，并证明细胞外基质的重组是迷幻药介导的关键期重新开放的一个共同下游机制。这些结果对在临床实践中实施迷幻药以及设计用于治疗神经精神疾病的新型化合物具有重要意义。

据了解，迷幻药是一类广泛的药物，其定义是能够诱发改变意识的状态。几千年来，这些药物一直被用于精神和医疗方面，最近的一些临床成功案例又激发了人们对开发迷幻药疗法的兴趣。然而，能够解释这些共同现象和治疗特性的统一机制仍然未知。

附：英文原文

Title: Psychedelics reopen the social reward learning critical period

Author: Nardou, Romain, Sawyer, Edward, Song, Young Jun, Wilkinson, Makenzie, Padovan-Hernandez, Yasmin, de Deus, Jnia Lara, Wright, Noelle, Lama, Carine, Faltin, Sehr, Goff, Loyal A., Stein-OBrien, Genevieve L., Dlen, Gl

Issue&Volume: 2023-06-14

Abstract: Psychedelics are a broad class of drugs defined by their ability to induce an altered state of consciousness1,2. These drugs have been used for millennia in both spiritual and medicinal contexts, and a number of recent clinical successes have spurred a renewed interest in developing psychedelic therapies3,4,5,6,7,8,9. Nevertheless, a unifying mechanism that can account for these shared phenomenological and therapeutic properties remains unknown. Here we demonstrate in mice that the ability to reopen the social reward learning critical period is a shared property across psychedelic drugs. Notably, the time course of critical period reopening is proportional to the duration of acute subjective effects reported in humans. Furthermore, the ability to reinstate social reward learning in adulthood is paralleled by metaplastic restoration of oxytocin-mediated long-term depression in the nucleus accumbens. Finally, identification of differentially expressed genes in the ‘open state’ versus the ‘closed state’ provides evidence that reorganization of the extracellular matrix is a common downstream mechanism underlying psychedelic drug-mediated critical period reopening. Together these results have important implications for the implementation of psychedelics in clinical practice, as well as the design of novel compounds for the treatment of neuropsychiatric disease.

DOI: 10.1038/s41586-023-06204-3

Source: https://www.nature.com/articles/s41586-023-06204-3