# Neural basis underlying the impact of stress on sleep

> **NIH NIH R01** · UNIVERSITY OF PENNSYLVANIA · 2024 · $588,018

## Abstract

PROJECT SUMMARY
Stress is associated with insufficient sleep and poor quality sleep. In particular, fragmented non-rapid eye
movement sleep (NREMs) due to frequent brief arousals (microarousals, MAs) disrupts sleep continuity, and
rapid eye movement sleep (REMs) abnormalities are often observed in patients with insomnia and depression.
Insufficient sleep and alterations in sleep microarchitecture caused by stress may in turn worsen the stress
symptoms, such as cognitive impairment, and have been shown to increase the risk of developing psychiatric
disorders. Nevertheless, the identity of the involved stress- and sleep-regulatory circuits, and the mechanisms
by which stress perturbs distinct features of the sleep architecture and negatively impacts cognitive behaviors
are still largely unclear. We have recently shown that acute psychosocial stress in mice decreases the amount
of sleep and disrupts sleep quality by causing frequent MAs and suppressing REMs. We propose that the
stress-induced decrease in the amount of sleep and changes in sleep microarchitecture are mediated by
different circuit mechanisms. The preoptic area of the hypothalamus (POA), a crucial center regulating macro-
and microarchitecture of sleep and wakefulness, is densely innervated by stress-regulatory noradrenergic
neurons in the locus coeruleus (NELC) and corticotropin-releasing hormone neurons in the paraventricular
nucleus (CRHPVN). The goal of this proposal is to investigate to what extent the NELC and CRHPVN neurons
cause stress-induced sleep disturbances and memory impairment via projections to distinct POA
subpopulations. Our central hypothesis is that stress-induced MAs and REMs dysregulation are mediated by
inputs from NELC neurons to the POA (NELC→POA), while the overall decrease in sleep is mediated by inputs
from CRHPVN neurons (CRHPVN→POA) and that reversing sleep disturbances attenuates stress-induced memory
deficits. Aim 1 will determine the role of NELC→POA projections in stress-induced MAs and REMs dysregulation
as well as related memory deficits. Aim 2 will determine the role of CRHPVN→POA projections in stress-induced
wakefulness and related memory deficits. Accomplishing these aims will provide important insights into the
neural basis of stress-induced sleep disturbances and the benefits of good quality and quantity sleep in
reversing stress symptoms, with potential relevance to understand and develop novel therapeutic interventions
for stress-related sleep disorders.

## Key facts

- **NIH application ID:** 11058766
- **Project number:** 1R01MH136491-01A1
- **Recipient organization:** UNIVERSITY OF PENNSYLVANIA
- **Principal Investigator:** Shinjae Chung
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $588,018
- **Award type:** 1
- **Project period:** 2024-09-18 → 2025-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11058766

## Citation

> US National Institutes of Health, RePORTER application 11058766, Neural basis underlying the impact of stress on sleep (1R01MH136491-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/11058766. Licensed CC0.

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