# Impact of juvenile social isolation on corticothalamic interactions controlling adult social behavior

> **NIH NIH F31** · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2021 · $44,436

## Abstract

Project Summary/Abstract
Social functioning deficits are associated with a variety of different disorders and represent a substantial public
health burden. Adult social functioning is strongly influenced by social experience during development and
social deficits are highly pronounced in neurodevelopmental disorders such as autism and schizophrenia,
which may reflect disrupted consolidation of social experience. Attempts to treat and prevent social deficits
have been largely unsuccessful. This is due, in part, to a lack of understanding of the brain network
mechanisms underlying social functioning and poor characterization of the experience-dependent
developmental processes responsible for maturation of social functioning.
This proposal aims to fill the gaps in our understanding of the neurobiological mechanisms governing social
behavior and social experience-dependent maturation. We employ a mouse juvenile social isolation (JSI)
paradigm to model disrupted social experience-dependent maturation and interrogate the neurobiological
bases of social deficits. JSI is known to reduce sociability and cause physiological abnormalities in the medial
prefrontal cortex (mPFC) in adulthood. Our recent findings suggest that neurons projecting from the mPFC to
the posterior paraventricular thalamus (mPFCpPVT neurons) play a key role in sociability and are selectively
impacted by JSI. We show that optogenetic stimulation of mPFCpPVT neurons rescues sociability in JSI
mice, raising the possibility that this circuit can be targeted for therapeutic purposes. However, it is unclear how
mPFCpPVT neurons influence broader brain network activity and ultimately affect social functioning.
Recent studies suggest that neural oscillations play a central role in coordinating the flow of information across
distributed brain networks during complex behaviors. mPFCpPVT neurons are well-positioned to generate
and synchronize corticothalamic oscillations. However, corticothalamic oscillations have not been explicitly
linked to social behavior. Therefore, the overarching hypothesis of this proposal is that mPFCpPVT neurons
facilitate corticothalamic oscillations that support social functioning, and that juvenile isolation will lead to a loss
of mPFCpPVT recruitment and corticothalamic synchrony during social behavior. To test this hypothesis, we
will conduct state-of-the-art electrophysiological recording of mPFC and pPVT activity with optogenetic tagging
of mPFCpPVT neurons during tests of social behavior. Further, we will explore the mechanisms underlying
rescue of JSI-induced sociability deficits mediated by optogenetic stimulation of mPFCpPVT neurons, asking
whether recovery of sociability is associated with restoration of normal mPFCpPVT recruitment and
corticothalamic synchrony during social behavior. Overall, this project will provide novel insight into the
neurobiological basis of social functioning and has the potential to inspire improved treatment and prevent...

## Key facts

- **NIH application ID:** 10313014
- **Project number:** 1F31MH127805-01
- **Recipient organization:** ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
- **Principal Investigator:** Michael Brian Leventhal
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $44,436
- **Award type:** 1
- **Project period:** 2021-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10313014

## Citation

> US National Institutes of Health, RePORTER application 10313014, Impact of juvenile social isolation on corticothalamic interactions controlling adult social behavior (1F31MH127805-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10313014. Licensed CC0.

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