The importance of oxytocin mechanisms in the control of mouse parturition.
The role of oxytocin in parturition in mice was investigated. Pup birth profiles, blood samples and brains were collected from parturient mice observed under red light conditions in a reversed light:dark photoperiod. Peripheral administration of an oxytocin antagonist in a dose-dependent manner delayed the birth of subsequent pups, indicating that oxytocin is required for a normal pup birth profile. Oxytocin neurones were activated during birth as shown by both increased immediate early gene ( Fos) expression in oxytocin neurones in the supraoptic nucleus and increased plasma oxytocin concentrations during birth. In addition, the nucleus of the tractus solitarius and the olfactory bulbs, sites that process inputs to oxytocin neurones, become activated during parturition. Exposure to stress during parturition halted subsequent deliveries; at this stage plasma oxytocin concentrations were not higher than those of virgin mice, and birth was restored by administration of oxytocin. Administration of beta-adrenergic antagonist (propranolol) also restored stress-delayed birth, whereas administration of ritrodrine (beta-agonist) delayed birth in non-stressed mice, indicating that adrenergic mechanisms contribute to stress-delayed births in mice. Administration of morphine (mu-opioid agonist) delayed births transiently, but naloxone (opioid antagonist) did not prevent stress-delayed birth, indicating that endogenous opioids do not appear to contribute to neuroendocrine or uterine mechanisms that promote birth in mice. Therefore, despite evidence in oxytocin knockout mice that oxytocin is not essential for parturition in this species, the results of the present study indicate that oxytocin neurone activity and secretion contribute to the birth process in normal mice.
Douglas
A J
AJ
Laboratory of Neuroendocrinology, Division of Biomedical and Clinical Laboratory Sciences, University of Edinburgh, EH8 9XD, UK. alison.j.douglas@ed.ac.uk
Leng
G
G
Russell
J A
JA
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D005260:Female; D015870:Gene Expression; D016762:Genes, fos; D007743:Labor, Obstetric / Q000187:drug effects / Q000378:metabolism*; D051379:Mice / Q000378:metabolism*; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010121:Oxytocin / Q000032:analysis / Q000502:physiology*; D011247:Pregnancy; D011433:Propranolol / Q000494:pharmacology; D017450:Receptors, Opioid, mu / Q000819:agonists; D012312:Ritodrine / Q000494:pharmacology; D013312:Stress, Physiological / Q000378:metabolism; D013495:Supraoptic Nucleus / Q000737:chemistry / Q000378:metabolism*
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D009292:Narcotic Antagonists; D017450:Receptors, Opioid, mu; D009270:Naloxone; D010121:Oxytocin; D009020:Morphine; D011433:Propranolol; D012312:Ritodrine