title: Opioids and coupling of the anterior peri-third ventricular input to oxytocin neurones in anaesthetized pregnant rats.
abstract: In the pregnant rat the osmotic drive to oxytocin neurones is reduced and oxytocin secretion itself is inhibited by endogenous opioids. Coupling of the anterior peri-third ventricular input pathway, involved in osmoregulation, to magnocellular oxytocin neurones was studied in urethane-anaesthetized virgin and 21 day pregnant rats using electrical stimulation of the region anterior and ventral to the third cerebral ventricle (AV3V region) to drive the oxytocin neurones, and giving naloxone to prevent the action of any endogenous opioids on the system. Trains of stimuli (0.5 mA, 1 ms pulses, 10 s on 10 s off, at either 10 Hz or 25 Hz for 10 or 2 min respectively) were given at 20 or 30 min intervals via an electrode stereotaxically-implanted in the AV3V region, and femoral arterial blood plasma samples collected immediately before and after each stimulation were radioimmunoassayed for oxytocin concentration. The first (control) AV3V stimulation increased plasma oxytocin concentration reproducibly and similarly in virgin and 21-day pregnant rats. Naloxone administered 10 min before the second stimulus increased basal plasma oxytocin concentration in virgin and pregnant rats and increased the oxytocin secretory response to 25 Hz AV3V stimulation in virgin but not pregnant rats, and the response was significantly greater in virgin rats. Naloxone reveals oxytocin secretion unrestrained by endogenous opioids, therefore it appears that there is an opioid-independent reduction in the excitatory coupling of the AV3V input to oxytocin neurones which may explain the reduced osmoresponsiveness of oxytocin neurones at the end of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Physiology, Edinburgh University Medical School, Scotland, UK.
authors.forename: P M
authors.initials: PM
authors.lastname: Bull
authors.forename: A J
authors.initials: AJ
authors.lastname: Douglas
authors.forename: J A
authors.initials: JA
authors.lastname: Russell
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D000700:Analgesics / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002552:Cerebral Ventricles / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D004558:Electric Stimulation; D005260:Female; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009294:Narcotics / Q000494:pharmacology*; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010121:Oxytocin / Q000502:physiology*; D011247:Pregnancy; D011759:Pyrrolidines / Q000494:pharmacology; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
chemical_list: D000700:Analgesics; D009294:Narcotics; D011759:Pyrrolidines; D009270:Naloxone; D010121:Oxytocin; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine