# A potential novel role for hippocampal subregion ventral CA2 in sociability

> **NIH NIH F30** · COLUMBIA UNIVERSITY HEALTH SCIENCES · 2021 · $46,041

## Abstract

Project Summary/Abstract
Social animals, including humans and rodents, have an inherent drive to seek out and create bonds with
conspecifics that benefit their survival. This drive for social contact is diminished in multiple human psychiatric
and neurological disorders, including autism spectrum disorders, schizophrenia, and depression. The
underlying brain structures and circuits that mediate sociability, defined as the preference and desire for social
interaction, are under intense investigation as researchers seek new targets for circuit-based interventions of
these disorders.
The hippocampus is a brain structure with crucial roles in memory and behavior. Appearing as an extended
“C”-shaped structure in rodents, the hippocampus can be further defined along its longitudinal (dorsoventral)
axis. The dorsal (dHPC) and ventral (vHPC) hippocampus are proposed to have different functional roles, with
dHPC regulating cognitive functions including spatial navigation and contextual memory, and vHPC influencing
emotional processing and anxiety. Inhibition of vHPC increases sociability in rodents, likely due to decreased
anxiety. Whether the hippocampus can influence sociability independently of anxiety remains unclear.
The hippocampus can be additionally subdivided into the Cornu Ammonis subfields CA1-CA4 along its
transverse axis. The hippocampal subregion CA2 has recently emerged as a crucial regulator of social
recognition memory (SRM) and behavior. Global knockout of genes that, in the hippocampus, are exclusively
expressed in CA2 results in decreased SRM, social aggression (SA), and sociability. In contrast, while acute or
chronic inhibition of the dorsal region of CA2 (dCA2) reduce SRM and SA, it does not alter sociability.
Given the importance of dCA2 in social memory and behavior, and the role of vHPC in emotional regulation, I
hypothesize that ventral CA2 (vCA2) may regulate sociability. My preliminary results indicate that acute
pharmacogenetic inhibition of vCA2 results in a significant reduction in sociability, without a concomitant
change in anxiety. I will test my hypothesis of a role for vCA2 in sociability through two aims: first, I will probe
the necessity and sufficiency of vCA2 in social- and non-social behaviors (Aim 1). I will then investigate the
underlying vCA2 projections and activity that are important for vCA2’s role in social behavior (Aim 2). Together,
these results will expand understanding of the brain circuits that underlie sociability, and potentially identify
vCA2 as a new target for treatment of disorders with reduced social interest.

## Key facts

- **NIH application ID:** 10168469
- **Project number:** 5F30MH120922-02
- **Recipient organization:** COLUMBIA UNIVERSITY HEALTH SCIENCES
- **Principal Investigator:** Lara Marie Boyle
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $46,041
- **Award type:** 5
- **Project period:** 2020-03-01 → 2024-02-29

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10168469

## Citation

> US National Institutes of Health, RePORTER application 10168469, A potential novel role for hippocampal subregion ventral CA2 in sociability (5F30MH120922-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10168469. Licensed CC0.

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