Opioid control of prolactin secretion in late pregnant rats is mediated by tuberoinfundibular dopamine neurons

Neurosci Lett. 2002 Aug 2;328(1):60-4. doi: 10.1016/s0304-3940(02)00431-7.

Abstract

Prolactin (PRL) secretion from the anterior pituitary is tonically inhibited by tuberoinfundibular dopamine (TIDA) neurons in the arcuate nucleus of the hypothalamus. During late pregnancy, TIDA neuronal activity is reduced allowing the expression of an antepartum PRL surge. We show here that continuous infusion of the opioid receptor antagonist naloxone (10 mg/h) during the night preceding parturition completely abolished the antepartum PRL surge and significantly increased TIDA neuronal activity. These data indicate that endogenous opioid neurons facilitate PRL secretion at the end of pregnancy by suppressing TIDA neuronal activity.

MeSH terms

  • 3,4-Dihydroxyphenylacetic Acid / metabolism
  • Animals
  • Arcuate Nucleus of Hypothalamus / drug effects
  • Arcuate Nucleus of Hypothalamus / metabolism*
  • Dopamine / metabolism*
  • Female
  • Hypothalamo-Hypophyseal System / drug effects
  • Hypothalamo-Hypophyseal System / metabolism*
  • Labor, Obstetric / metabolism*
  • Median Eminence / drug effects
  • Median Eminence / metabolism
  • Naloxone / pharmacology
  • Narcotic Antagonists / pharmacology
  • Neural Inhibition / drug effects
  • Neural Inhibition / physiology*
  • Neurons / drug effects
  • Neurons / metabolism*
  • Opioid Peptides / metabolism*
  • Pregnancy / metabolism*
  • Prolactin / blood
  • Prolactin / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Up-Regulation / drug effects
  • Up-Regulation / physiology

Substances

  • Narcotic Antagonists
  • Opioid Peptides
  • 3,4-Dihydroxyphenylacetic Acid
  • Naloxone
  • Prolactin
  • Dopamine