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Hypothalamic prolactin receptor+ dopaminergic neurons regulate energy metabolism and nociceptive threshold in mice during lactation
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DOI：10.1038/s41467-026-76678-y.png)
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Abstract
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Women during lactation undergo significant bone loss and metabolic changes. However, the underlying mechanisms in the brain remain unclear. Herein, we found that prolactin receptor (PRLR)+ neurons in the hypothalamus control lactation physiology and metabolism in mice. Prolactin induces tyrosine hydroxylase (Th) expression in PRLR+ dopaminergic neurons of the arcuate nucleus (ARC). Interestingly, neuropeptide Y (NPY) expression was elevated to alter energy demand and nociceptive threshold during lactation. Knocking down either PRLR or NPY in the ARC significantly reduced food demand and nociceptive threshold. Importantly, in addition, prolactin also induces Th expression in the hypothalamic paraventricular nucleus (PVN) to increase sympathetic outflow to mobilize Ca2+ in bone. Importantly, brain-derived osteoanabolic hormone communication network factor 3 (CCN3) is downstream of PRLR signaling in the dopaminergic neurons. Thus, hypothalamic PRLR+ neurons identified in the current study regulate bone and fat metabolism, nociceptive threshold, and energy demand in mice during lactation. The mechanisms by which the brain controls maternal metabolism through hormones remain unclear. Here, authors find PRLR+ dopaminergic neurons in the hypothalamus regulate bone and fat metabolism and alter nociceptive threshold through NPY in lactating mice.
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