4.5 Article

A subpopulation of oxytocin neurons initiate expression of CRF receptor 1 (CRFR1) in females post parturition

Journal

PSYCHONEUROENDOCRINOLOGY
Volume 145, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2022.105918

Keywords

Oxytocin (OT); Stress; Corticotropin releasing factor (CRF); Corticotropin releasing hormone (CRH); Corticotropin releasing factor receptor 1; (CRFR1); Postpartum depression

Funding

  1. Welch Foundation
  2. National Institutes of Health (NIH, USA): National Institute of Mental Health (NIMH) [R56MH114032, R01MH112768, R15MH118692]

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Oxytocin is crucial for successful reproduction and maternal behavior. This study reveals that a subset of oxytocin neurons express the stress neuropeptide receptor CRFR1 in reproductive females. The expression of CRFR1 increases during the postpartum period and is maintained even after breeding ceases. This finding suggests a mechanism by which stress can influence oxytocin release and promote stress resilience in mothers.
Oxytocin (OT) is essential for successful reproduction, particularly during parturition and lactation. During the postpartum period, OT also influences maternal behavior to promote bonding between mothers and their newborns, and increases stress resilience. However, the mechanism by which stress influences OT neuron activity and OT release has remained unclear. Here, we provide evidence that a subpopulation of OT neurons initiate expression of the receptor for the stress neuropeptide Corticotropin Releasing Factor (CRF), CRFR1, in repro-ductive females. OT neuron expression of CRFR1 begins at the first parturition and increases during the post-partum period until weaning. The percentage of OT neurons that express CRFR1 increases with successive breeding cycles until it reaches a plateau of 20-25% of OT neurons. OT neuron expression of CRFR1 in repro-ductive females is maintained after they are no longer actively breeding. CRFR1 expression leads to activation of OT neurons when animals are stressed. We propose a model in which direct CRF signaling to OT neurons selectively in reproductive females potentiates OT release to promote stress resilience in mothers.

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