Rapid estradiol-17beta modulation of opioid actions on the electrical and secretory activity of rat oxytocin neurons in vivo.

Abstract:

: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.

journal_name

Neurochem Res

journal_title

Neurochemical research

authors

Brown CH,Brunton PJ,Russell JA

doi

10.1007/s11064-007-9506-7

subject

Has Abstract

pub_date

2008-04-01 00:00:00

pages

614-23

issue

4

eissn

0364-3190

issn

1573-6903

journal_volume

33

pub_type

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