Elevated prolactin during pregnancy drives a phenotypic switch in mouse hypothalamic dopaminergic neurons

Research output: Contribution to journalArticlepeer-review


  • Siew Yip
  • Nicola Romano
  • Papillon Gustafson
  • Eloise Williams
  • Ilona Kokay
  • Agnes O Martin
  • Patrice Mollard
  • David Grattan
  • Stephen Bunn

Colleges, School and Institutes


Altered physiological states require neuronal adaptation. In late pregnancy and lactation, a sub-population of the mouse hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons alters their behavior to synthesize and release met-enkephalin rather than dopamine. These neurons normally release dopamine to inhibit prolactin secretion and are activated by prolactin in a short-loop feedback manner. In lactation, dopamine synthesis is suppressed in an opioid-dependent (naloxone-reversible) manner, meaning that prolactin secretion is disinhibited. Conditional deletion of the prolactin receptor in neurons reveals that this change in phenotype appears to be driven by prolactin itself, apparently through an alteration in intracellular signaling downstream of the prolactin receptor that favors enkephalin production instead of dopamine. Thus, prolactin effectively facilitates its own secretion, which is essential for lactation and maternal behavior. These studies provide evidence of a physiologically important, reversible alteration in the behavior of a specific population of hypothalamic neurons in the adult brain.


Original languageEnglish
Pages (from-to)1787-1799
JournalCell Reports
Issue number7
Early online date12 Feb 2019
Publication statusE-pub ahead of print - 12 Feb 2019


  • dopamine, encephalin, hypothalamus, lactation, lactotrophs, neuronal plasticity, prolactin, prolactin receptor, tuberoinfundibular dopaminergic neurons