研究发现，LSD通过与自闭症相关的蛋白质促进社会行为

研究发现，LSD通过与自闭症相关的蛋白质促进社会行为

The authors of a new study into the behavioral effects of LSD have suggested that the drug may provide the key to developing new therapies for autism (ASD) and social anxiety. This assertion is based on the finding that LSD boosts social behavior in mice and that this effect is mediated by a protein complex that is often associated with ASD.

一项关于LSD行为效应的新研究的作者提出，这种药物可能为开发治疗自闭症(ASD)和社交焦虑的新疗法提供关键。这一论断是基于一项发现，即LSD促进老鼠的社会行为，而这种影响是由一种通常与自闭症谱系障碍有关的蛋白质复合物介导的。

Publishing their work in the Proceedings of the National Academy of Sciences, the researchers reveal that a single low dose of LSD had no effect on the rodents’ sociability, but that the animals became increasingly convivial towards unfamiliar mice after receiving the drug every day for a week. It is well known that LSD and other psychedelics produce their effects by interacting with serotonin receptors in the prefrontal cortex, and the study authors were, therefore, unsurprised to find that blocking these receptors nullified this increase in social behavior.

研究人员在《美国国家科学院院刊》(Proceedings of the National Academy of Sciences)上发表了他们的研究成果，他们揭示，单次低剂量的LSD对啮齿类动物的社交能力没有影响，但在连续一周每天服用这种药物后，这些动物对陌生的老鼠变得越来越友好。众所周知，LSD和其他致幻剂是通过与前额叶皮层的5 -羟色胺受体相互作用来产生效果的，因此，研究作者发现阻断这些受体会抵消社会行为的增加并不感到惊讶。

A similar effect was seen when the study authors blocked a second type of receptor, known as AMPA, in the animals’ prefrontal cortex, indicating that the social enhancement produced by LSD relies on both of these key receptor types.

当研究作者阻断动物前额叶皮层的第二种受体AMPA时，也看到了类似的效果，这表明LSD产生的社交增强依赖于这两种关键受体类型。

Benjamin Taub

Intriguingly, a number of psychedelic drugs have previously been shown to increase the activation of a protein complex called mTORC1, which regulates the sensitivity of serotonin and AMPA receptors. This compound is of particular interest as several studies have shown that dysregulation of mTORC1 causes alterations in brain activity that are linked to ASD and a range of social anxiety disorders.

有趣的是，许多迷幻药之前已经被证明可以增加一种叫做mTORC1的蛋白质复合物的激活，它调节5 -羟色胺和AMPA受体的敏感性。这种化合物特别有趣，因为一些研究表明mTORC1的失调会导致与ASD和一系列社会焦虑障碍相关的大脑活动的改变。

Using molecular analytics tools, the study authors verified that the regular administration of LSD produced an increase in mTORC1 activation in the rodents’ prefrontal cortices, suggesting a role for this important compound in regulating the social effects of psychedelics.

利用分子分析工具，研究作者证实了定期服用LSD会增加啮齿类动物前额皮质的mTORC1激活，表明这种重要化合物在调节迷幻剂的社会效应方面发挥了作用。

To investigate further, the researchers repeated their experiment using mice that had been genetically modified to lack a key ingredient of the mTORC1 protein complex and found that this eliminated the ability of LSD to enhance social behavior. This finding indicates that mTORC1 is a vital mediator of the behavioral effects of LSD, and that its role in tweaking the activity of serotonin and AMPA receptors may help to explain certain neurological disorders.

为了进一步调查，研究人员重复了他们的实验，使用的老鼠是经过基因改造的，以缺乏一种关键成分的mTORC1蛋白质复合物，并发现这消除了LSD增强社会行为的能力。这一发现表明mTORC1是LSD行为效应的重要中介，它在调节5 -羟色胺和AMPA受体活性方面的作用可能有助于解释某些神经障碍。

Based on this outcome, the study authors state that the interaction between mTORC1, serotonin receptors and AMPA receptors represents a promising avenue of research and that the effects of LSD and other psychedelics “should be explored for the treatment of mental diseases with [social behavior] impairments such as autism spectrum disorder and social anxiety disorder.”

基于这一结果,该研究的作者指出，mTORC1、5 -羟色胺受体和AMPA受体之间的相互作用代表了一个有前途的研究途径，以及LSD和其他致幻剂的作用“应该探索用于治疗带有(社会行为)障碍的精神疾病，如自闭症谱系障碍和社交焦虑障碍。”