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Rapid Estradiol-17β Modulation of Opioid Actions on the Electrical and Secretory Activity of Rat Oxytocin Neurons In vivo

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)614-623
Number of pages10
JournalNeurochemical Research
Issue number4
Publication statusPublished - Apr 2008


During pregnancy, emergence of endogenous opioid inhibition of oxytocin neurons is revealed by increased oxytocin secretion after administration of the opioid receptor antagonist, naloxone. Here we show that prolonged estradiol-17beta and progesterone treatment (mimicking pregnancy levels) potentiates naloxone-induced oxytocin secretion in urethane-anesthetized virgin female rats. We further show that estradiol-17beta alone rapidly modifies opioid interactions with oxytocin neurons, by recording their firing rate in anesthetized rats sensitized to naloxone by morphine dependence. Naloxone-induced morphine withdrawal strongly increased the firing rate of oxytocin neurons in morphine dependent rats. Estradiol-17beta did not alter basal oxytocin neuron firing rate over 30 min, but amplified naloxone-induced increases in firing rate. Firing pattern analysis indicated that acute estradiol-17beta increased oxytocin secretion in dependent rats by increasing action potential clustering without an overall increase in firing rate. Hence, rapid estradiol-17beta actions might underpin enhanced oxytocin neuron responses to naloxone in pregnancy.

    Research areas

  • Action Potentials, Analgesics, Opioid, Animals, Electrophysiology, Estradiol, Female, Morphine Dependence, Naloxone, Narcotic Antagonists, Neurons, Oxytocin, Radioimmunoassay, Rats, Rats, Sprague-Dawley, Receptors, Opioid, mu, Substance Withdrawal Syndrome

ID: 107005