Smith A S, Williams Avram S K, Cymerblit-Sabba A, Song J, Young W S
Section on Neural Gene Expression, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
Mol Psychiatry. 2016 Aug;21(8):1137-44. doi: 10.1038/mp.2015.189. Epub 2016 Jan 5.
Social cognition enables individuals to understand others' intentions. Social memory is a necessary component of this process, for without it, subsequent encounters are devoid of any historical information. The CA2 area of the hippocampus, particularly the vasopressin 1b receptor (Avpr1b) expressed there, is necessary for memory formation. We used optogenetics to excite vasopressin terminals, originating from the hypothalamic paraventricular nucleus, in the CA2 of mice. This markedly enhanced their social memory if the stimulation occurred during memory acquisition, but not retrieval. This effect was blocked by an Avpr1b antagonist. Finally, this enhanced memory is resistant to the social distraction of an introduced second mouse, important for socially navigating populations of individuals. Our results indicate the CA2 can increase the salience of social signals. Targeted pharmacotherapy with Avpr1b agonists or deep brain stimulation of the CA2 are potential avenues of treatment for those with declining social memory as in various dementias.
社会认知使个体能够理解他人的意图。社会记忆是这一过程的必要组成部分，因为没有它，后续的相遇就缺乏任何历史信息。海马体的CA2区域，特别是该区域表达的血管加压素1b受体（Avpr1b），对记忆形成是必需的。我们使用光遗传学来刺激源自下丘脑室旁核的血管加压素终末，这些终末位于小鼠的CA2区。如果在记忆获取过程中进行刺激，这会显著增强它们的社会记忆，但在记忆检索时则不会。这种效应被Avpr1b拮抗剂阻断。最后，这种增强的记忆对引入的第二只小鼠的社会干扰具有抗性，这对于在个体群体中进行社交导航很重要。我们的结果表明，CA2可以增加社会信号的显著性。用Avpr1b激动剂进行靶向药物治疗或对CA2进行深部脑刺激是治疗各种痴呆症中社会记忆衰退患者的潜在途径。
