# Role of early-life sleep and sensory environment in shaping the development of affiliative behavior and PV-interneurons in the somatosensory cortex of the highly social prairie vole.

> **NIH NIH F31** · OREGON HEALTH & SCIENCE UNIVERSITY · 2024 · $48,974

## Abstract

Project Summary
Early life sleep is fundamental to the development of affiliative behavior, defined as any behavioral display that
promotes positive social engagement. Autism spectrum disorder (ASD) is characterized by persistent changes
in social behavior, sensory sensitivity, and sleep disruption. Additionally, excitatory, and inhibitory neuronal
activity (E/I balance) is altered in ASD. Increased expression of parvalbumin-positive inhibitory interneurons and
the appearance of extracellular structures, perineuronal nets (PNNs) surrounding these cells mark the functional
maturation of the sensory cortex. The highly social prairie vole is an excellent model with which to study the
relationship between early-life sleep and the development of neural circuitry underlying the display of affiliative
behavior. Unlike mice and rats, prairie voles demonstrate species-typical familiarity preference demonstrated by
side-by-side huddling in a novel environment. Our lab has shown early-life sleep disruption (ELSD) in prairie
voles impairs species-typical affiliative behavior (huddling) and increases PV interneurons (PVIs) in the
somatosensory cortex of adults. However, we do not know how ELSD impacts the early display of affiliative
behavior nor how PV interneurons may mediate this early behavioral development. Our understanding of
social behavior has been largely limited to manual scoring using a fixed set of identifiers. Use of novel
computational tools for the objective discovery of affiliative behavior will allow for a more comprehensive
understanding of subtle cues in this complex behavior during development. Thus, I propose to investigate the
development of affiliative behavior between same-sex siblings (Aim 1) and PVIs (Aim 2) of male and female
prairie voles across adolescence (P28-42) following ELSD (P14-21) or the Control condition. Characterizing the
trajectory of both brain and behavior is expected to provide key insights into the functional role of early-life sleep
in social development. The central hypothesis of this work is that, early-life sleep disruption alters the
maturation of PV interneurons and results in reduced affiliative behavior between siblings during
development. To understand the mechanisms underlying the timing of PV expression and affiliative behavior,
we will randomize animals to standard housing versus an enriched environment (Aim 3) to probe potential rescue
of brain and behavioral changes induced by ELSD. Identifying the molecular trajectories by which ELSD
changes typical affiliative behavior and how enrichment modifies these social impairments may enable
a better understanding of mechanisms underlying successful therapies for children with ASD.

## Key facts

- **NIH application ID:** 10995110
- **Project number:** 1F31MH136684-01A1
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Noah Emery Pollak Milman
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $48,974
- **Award type:** 1
- **Project period:** 2024-12-01 → 2027-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10995110

## Citation

> US National Institutes of Health, RePORTER application 10995110, Role of early-life sleep and sensory environment in shaping the development of affiliative behavior and PV-interneurons in the somatosensory cortex of the highly social prairie vole. (1F31MH136684-01A1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/10995110. Licensed CC0.

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