Original Article

Molecular Psychiatry (2016) 21, 1137–1144; doi:10.1038/mp.2015.189; published online 5 January 2016

Targeted activation of the hippocampal CA2 area strongly enhances social memory

A S Smith1, S K Williams Avram1, A Cymerblit-Sabba1, J Song1 and W S Young1

1Section on Neural Gene Expression, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA

Correspondence: Dr AS Smith or Dr WS Young, Section on Neural Gene Expression, National Institute of Mental Health, National Institutes of Health, 9000 Rockville Pike, Building 49, Room 5A56, Bethesda, MD 20892, USA. E-mail: adam.smith@nih.gov or wsy@mail.nih.gov

Received 14 August 2015; Revised 10 October 2015; Accepted 5 November 2015
Advance online publication 5 January 2016

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Abstract

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.