Investigates prolactin's effect on REM sleep during stress in mice, suggesting hormonal regulation of sleep responses.
*Corresponding author e-mail: kpaul@msm.edu Introduction: The present study was undertaken to investigate the link between hormonal stress response mechanisms and the changes in sleep associated with psychogenic stressors. Both REM sleep and prolactin levels are increased in rodents following restraint stress. This suggests prolactin may be involved in the ability of restraint stress to increase REM sleep amount. Methods: In the current study, we examined sleep following restraint stress in cabergoline treated mice. Cabergoline is a dopamine D2 agonist that is in clinical use as a prolactin release inhibitor. Male C57BL/6J mice (3-4 months of age) were implanted with EEG/EMG recording electrodes and placed in 12:12 LD. After acclimation to the sleep recording apparatus, mice received an i.p. injection of either 0.25 mg/kg cabergoline or vehicle prior to 1-hr of restraint stress during the light phase (ZT 5-6) and allowed an 18-hr recovery opportunity. Polysomnograms were hand scored for REM sleep and data were analyzed using ANOVA to detect between and within factor differences. Restraint stress elicited a significantly smaller increase in REM sleep amount when animals were pretreated with cabergoline. Results: REM sleep amount in restrained mice pretreated with cabergoline (44.0 min) was less than (p < .05 ;dark phase ZT 12-24) restrained mice pretreated with vehicle (72.3 min). Cabergoline also decreased REM sleep amount during the light phase and early part of the dark phase in non-restrained animals. This sleep loss resulted in a REM sleep rebound in the latter half of the dark phase. Our data demonstrate that the inhibition of prolactin secretion reduces the REM sleep amount increase induced by restraint. Our results also indicate that baseline REM sleep amount during the rest phase is partially dependent on prolactin This is inferred from the ability of cabergoline to reduce light phase REM sleep in non-restrained animals. Conclusion: Collectively, these data demonstrate the importance of prolactin as a sleep regulator, and as a mediator of the ability of stress to alter REM sleep. In addition, prolactin levels exhibit a sexual dimorphism in which adult females have higher basal prolactin levels. Thus these data also support the hypothesis that sex differences in the ability of restraint stress to alter sleep are dependent on prolactin. Support: NINDS award NS34194 and STC Program of the National Science Foundation under Agreement No. IBN-9876754. Publication History Article published online: 16 June 2026 © 2009. Brazilian Sleep Academy. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/) Thieme Revinter Publicações Ltda. Rua Rego Freitas, 175, loja 1, República, São Paulo, SP, CEP 01220-010, Brazil
No takes yet. Share an insight, caveat, or question.
Paul et al. (2009) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: