# Neural Mechanisms Linking Sensory Perception and Social Behavior

> **NIH NIH R01** · YALE UNIVERSITY · 2023 · $424,474

## Abstract

PROJECT SUMMARY
 Abnormalities in sensory perception are prevalent features in individuals with autism spectrum disorders
(ASD), accompanying the core social deficits. A central challenge in autism research is to identify alterations in
neurobiological mechanisms that underlie processes as distinct as sensory perception and social cognition. As
such, our long-term goal is to understand common developmental and circuit mechanisms shared by sensory
and social information processing. Considerable evidence indicates that the neuropeptide oxytocin significantly
contributes to a wide range of social behaviors, and more recently, it has been linked to synaptic plasticity in
sensory cortices during development. These findings raise an exciting but untested possibility that oxytocin
signaling is associated with both tactile processing and social function. In our preliminary studies, we found that
oxytocin receptors (OXTRs) are expressed abundantly and specifically in the somatostatin-expressing
interneurons (SST INs) in the primary somatosensory cortex (S1) during development. Activating OXTRs
selectively and strongly depolarizes SST INs, while OXTR deletion in these neurons leads to hyperpolarization
of the resting membrane potential and reduced in vivo network activity in the developing S1. In addition, mice
with targeted OXTR deletion in SST INs show impaired texture discrimination and sensory sensitivity, as well as
deficits in social preference. Based on these preliminary results, we hypothesize that oxytocin is required for
establishing proper synaptic connectivity in the developing somatosensory cortex, and that impairment in
oxytocin signaling leads to both tactile sensory abnormalities and social deficits. We will leverage our novel
longitudinal 2-photon imaging technique, electrophysiological and genetic approaches to identify the cell-type
specific role of oxytocin in the development of S1 and during acute social interactions through three aims. We
will assess the effects of oxytocin on the growth and survival of SST INs, as well as the maturation of circuit
connectivity in the developing S1 (Aim 1). We will dissect the role of oxytocin signaling in general tactile sensory
processing, and in encoding social cues during social contacts (Aim 2). We will explore the behavioral outcomes
of oxytocin signaling dysfunction and their neural corelates, and test if developmental tactile dysfunction as a
result of OXTR deletion exacerbates social deficits (Aim 3). Together, the results are expected to reveal common
neural mechanisms underlying sensory and social information processing, providing insights into basic rules for
brain circuit development, as well as identifying early diagnostic markers associated with ASD and other mental
disorders that can guide novel therapeutics.

## Key facts

- **NIH application ID:** 10717481
- **Project number:** 1R01NS133434-01
- **Recipient organization:** YALE UNIVERSITY
- **Principal Investigator:** Alicia Yue Che
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $424,474
- **Award type:** 1
- **Project period:** 2023-07-01 → 2028-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10717481

## Citation

> US National Institutes of Health, RePORTER application 10717481, Neural Mechanisms Linking Sensory Perception and Social Behavior (1R01NS133434-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10717481. Licensed CC0.

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