Related Experiment Video
Updated: Aug 21, 2026
Establishing a Device for Sleep Deprivation in Mice
Published on: September 22, 2023
Mice deficient in the interferon type I receptor have reduced REM sleep and altered hypothalamic hypocretin,
S G Bohnet1, T R Traynor, J A Majde
1Department of VCAPP College of Veterinary Medicine Washington State University PO Box 646520 Pullman, WA 99164-6520, USA.
Abstract:
We report that mice with a targeted null mutation in the interferon type I receptor (IFN-RI), which cannot respond to such IFNs as IFNalpha and IFNbeta, have a 30% reduction in time spent in spontaneous rapid eye movement sleep (REMS) as a consequence of a reduced number of REMS episodes. Time spent in nonrapid eye movement sleep (NREMS) was essentially unaltered in IFN-RI knockouts (KOs) compared to 129 SvEv controls. Body temperature and locomotor activity were similar in both strains of mice. Hypothalamic expression of mRNAs for molecules previously linked to sleep-wake regulation and an IFN-inducible antiviral gene, 2',5'-oligoadenylate synthetase 1a (OAS), were determined by real-time reverse-transcriptase polymerase chain reaction (RT2-PCR). The level of hypocretin A mRNA was elevated in IFN-RI KO mice compared to 129 SvEv mice, while prolactin mRNA and OAS mRNA levels were suppressed. Vasoactive intestinal peptide (VIP) and corticotropin-releasing hormone (CRH) mRNA levels were unchanged relative to controls. Serum prolactin levels were similar in both strains. Results are consistent with the hypothesis that increased hypocretin and reduced prolactin in the hypothalamus of IFN-RI KO mice are responsible for their reduced REMS. In addition, the reduced OAS expression may result in modulation of prolactin receptor signaling and thus contribute to suppression of REMS.
Insights
Mice lacking interferon type I receptor (IFN-RI) signaling show reduced rapid eye movement sleep (REMS). This sleep reduction is linked to altered hypothalamic hypocretin and prolactin levels in these mice.
Area of Science:
- Neuroscience
- Immunology
- Sleep Science
Background:
- Interferon type I (IFN-I) signaling plays a role in immune responses.
- The relationship between immune signaling and sleep regulation is not fully understood.
- IFN-I receptors (IFN-RI) mediate cellular responses to IFN-alpha and IFN-beta.
Purpose of the Study:
- To investigate the role of IFN-RI signaling in sleep regulation.
- To determine the impact of IFN-RI deficiency on sleep architecture in mice.
- To explore the underlying molecular mechanisms in the hypothalamus.
Main Methods:
- Utilized IFN-RI knockout (KO) mice and wild-type controls (129 SvEv).
- Measured sleep patterns, specifically REMS and NREMS, using established methods.
- Quantified hypothalamic mRNA expression of key regulatory molecules (hypocretin, prolactin, OAS, VIP, CRH) via RT2-PCR.
Main Results:
- IFN-RI KO mice exhibited a 30% reduction in REMS duration, primarily due to fewer REMS episodes.
- NREMS duration, body temperature, and locomotor activity remained comparable between KO and control mice.
- Hypothalamic analysis revealed elevated hypocretin A mRNA and suppressed prolactin and OAS mRNA in IFN-RI KO mice.
Conclusions:
- Impaired IFN-RI signaling leads to reduced REMS in mice.
- Increased hypothalamic hypocretin and decreased prolactin likely contribute to REMS suppression.
- Reduced OAS expression may further modulate prolactin signaling, impacting REMS.
