Pregnancy damps thermoregulatory rhythms across timescales through neural estrogen signaling in mice.

Authors

Laura R Cortes, Lingyun Xiong, Adriana R Vree, Fernando M C V Reis, Natalie Kim, Bing Feng, Mia R Hansen, Sakina Rashid, Norma P Sandoval, Julissa I Lopez, Yanlin He, Avishek Adhikari, J Edward van Veen, Alan Garfinkel, Eric J Deeds, Christopher S Colwell, Stephanie M Correa

Published in

Proceedings of the National Academy of Sciences of the United States of America. Volume 123. Issue 39. Pages e2611415123. Sep 29, 2026. Epub Sep 21, 2026.

Abstract

Pregnancy induces widespread physiological adaptations, including changes to core temperature (T_c), that may reduce fetal heat stress and enhance metabolic stability. Despite the potential importance of maternal thermoregulatory changes, the neural mechanisms organizing homeostatic rhythms during pregnancy remain poorly understood. Here, we demonstrate that pregnancy profoundly reshapes thermoregulatory dynamics across diurnal and ultradian timescales and that these changes are partially orchestrated by estrogen receptor alpha (ERα) signaling in neurons of the medial preoptic area (MPO^ERɑ). Using in vivo calcium recordings of MPO^ERɑ neurons, we show that MPO^ERɑ neural activity is synchronized with T_c oscillations in nonpregnant mice. Notably, this synchronization is lost during pregnancy and reemerges after parturition, indicating that MPO^ERɑ activity and T_c are synchronized in a manner that is dependent on reproductive state. Using chemogenetic inhibition, we show that MPO^ERɑ neurons are required for the lowering of T_c in late pregnancy. Using a genomic estrogen signaling reporter, we demonstrate that MPO^ERɑ neurons exhibit enhanced estrogen signaling in late pregnancy. This estrogen signaling helps coordinate maternal T_c changes, as selectively ablating ERα expression in the MPO increased T_c and its circadian and ultradian rhythmicity. Finally, we show that manipulating MPO^ERɑ cell activity and MPO Esr1 expression affected neonates: Silencing MPO^ERɑ neurons led to premature birth, while both silencing and gene ablation led to sex-specific changes to offspring body mass. In summary, these findings reveal a global suppression of T_c circadian and ultradian rhythmicity during pregnancy and identify ERα as a central modulator of these rhythms with consequences for fetal development.

PMID:
42766745
Bibliographic data and abstract were imported from PubMed on 22 Sep 2026.

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