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Altered sleep latency and arousal regulation in mice lacking norepinephrine.
Pharmacol Biochem Behav. 2004 Aug; 78(4):765-73.PB

Abstract

Latency to sleep and the amount of sensory stimulation required to awaken an animal are measures of arousal threshold, which are ultimately modulated by an arousal regulation system involving many brain areas. Among these brain areas and network connections are wake-promoting nuclei of the brainstem and their corresponding neurotransmitters, including norepinephrine (NE). In this study, we used mice that are unable to produce NE to study its role in regulating sleep latency after a variety of interventions, and to study arousal from sleep after sleep deprivation (SD). Sleep latency was measured after gentle awakening or after injections of saline, caffeine or modafinil. Sleep latency was also measured before and after partial restoration of NE pharmacologically. Arousal threshold was measured by recording the number of decibels of white noise required to wake each mouse from NREM sleep after 0, 3 and 3 + 3 h SD (3 h SD followed by < 2 min sleep, followed by an additional 3 h SD). Results showed that when mice were awakened without being touched, there were no differences in sleep latency between the genotypes. However, after an injection of saline, the control mice increased their sleep latency, whereas the NE-deficient mice did not. There were no group differences in sleep latency after treatment with either stimulant. The sleep latency difference between the genotypes was ameliorated by partial restoration of NE. The arousal threshold experiments revealed that significantly more noise was required to wake the NE-deficient mice after 3 and 3 + 3 h of SD. These findings show that mice lacking NE fall asleep more rapidly only after a mild stressor, such as an intraperitoneal injection. NE-deficient mice are also more difficult to wake up using audio stimulation after SD. The results presented here suggest that NE promotes wakefulness during transitions between sleep and wake under conditions involving mild stress and SD, but not under baseline circumstances.

Authors+Show Affiliations

Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195-7370, USA. melissa.hunsley@ucsf.eduNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15301933

Citation

Hunsley, Melissa S., and Richard D. Palmiter. "Altered Sleep Latency and Arousal Regulation in Mice Lacking Norepinephrine." Pharmacology, Biochemistry, and Behavior, vol. 78, no. 4, 2004, pp. 765-73.
Hunsley MS, Palmiter RD. Altered sleep latency and arousal regulation in mice lacking norepinephrine. Pharmacol Biochem Behav. 2004;78(4):765-73.
Hunsley, M. S., & Palmiter, R. D. (2004). Altered sleep latency and arousal regulation in mice lacking norepinephrine. Pharmacology, Biochemistry, and Behavior, 78(4), 765-73.
Hunsley MS, Palmiter RD. Altered Sleep Latency and Arousal Regulation in Mice Lacking Norepinephrine. Pharmacol Biochem Behav. 2004;78(4):765-73. PubMed PMID: 15301933.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Altered sleep latency and arousal regulation in mice lacking norepinephrine. AU - Hunsley,Melissa S, AU - Palmiter,Richard D, PY - 2003/09/19/received PY - 2004/05/12/revised PY - 2004/05/17/accepted PY - 2004/8/11/pubmed PY - 2005/3/5/medline PY - 2004/8/11/entrez SP - 765 EP - 73 JF - Pharmacology, biochemistry, and behavior JO - Pharmacol Biochem Behav VL - 78 IS - 4 N2 - Latency to sleep and the amount of sensory stimulation required to awaken an animal are measures of arousal threshold, which are ultimately modulated by an arousal regulation system involving many brain areas. Among these brain areas and network connections are wake-promoting nuclei of the brainstem and their corresponding neurotransmitters, including norepinephrine (NE). In this study, we used mice that are unable to produce NE to study its role in regulating sleep latency after a variety of interventions, and to study arousal from sleep after sleep deprivation (SD). Sleep latency was measured after gentle awakening or after injections of saline, caffeine or modafinil. Sleep latency was also measured before and after partial restoration of NE pharmacologically. Arousal threshold was measured by recording the number of decibels of white noise required to wake each mouse from NREM sleep after 0, 3 and 3 + 3 h SD (3 h SD followed by < 2 min sleep, followed by an additional 3 h SD). Results showed that when mice were awakened without being touched, there were no differences in sleep latency between the genotypes. However, after an injection of saline, the control mice increased their sleep latency, whereas the NE-deficient mice did not. There were no group differences in sleep latency after treatment with either stimulant. The sleep latency difference between the genotypes was ameliorated by partial restoration of NE. The arousal threshold experiments revealed that significantly more noise was required to wake the NE-deficient mice after 3 and 3 + 3 h of SD. These findings show that mice lacking NE fall asleep more rapidly only after a mild stressor, such as an intraperitoneal injection. NE-deficient mice are also more difficult to wake up using audio stimulation after SD. The results presented here suggest that NE promotes wakefulness during transitions between sleep and wake under conditions involving mild stress and SD, but not under baseline circumstances. SN - 0091-3057 UR - https://www.unboundmedicine.com/medline/citation/15301933/Altered_sleep_latency_and_arousal_regulation_in_mice_lacking_norepinephrine_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091305704001674 DB - PRIME DP - Unbound Medicine ER -