scholarly journals Do oxytocin neurones affect feeding?

Author(s):  
Amy A. Worth ◽  
Simon M. Luckman
Keyword(s):  
Analgesia ◽  
1995 ◽  
Vol 1 (4) ◽  
pp. 335-338
Author(s):  
Colin H. Brown ◽  
Niall P. Murphy ◽  
Gareth Leng ◽  
John A. Russell

Reproduction ◽  
2002 ◽  
pp. 543-552 ◽  
Author(s):  
AJ Douglas ◽  
G Leng ◽  
JA Russell

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.


2001 ◽  
Vol 11 (12) ◽  
pp. 935-939 ◽  
Author(s):  
Young ◽  
Iacangelo ◽  
Luo ◽  
King ◽  
Duncan ◽  
...  

1992 ◽  
Vol 70 (1) ◽  
pp. 100-105 ◽  
Author(s):  
Savio W. T. Cheng ◽  
William G. North

Peripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol∙min−1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 ± 2 to 290 ± 2 mosmol/kg H2O, p < 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation. The slopes of the relationship between the rise in [VP-RNP] (A[VP-RNP]) and the rise in Posm (ΔPosm) for the groups receiving pretreatment of 1 nmol OT (n = 5), 10 nmol OT (n = 7), and vehicle (n = 7) were similar (6.1 ± 1.4, r = 0.86; 5.1 ± 0.9, r = 0.91; and 6.6 ± 0.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93, respectively). For the 1-nmol dose of OT that generated plasma OT levels in the physiological range, the slopes of the relationship between the rise in [OT-RNP] (Δ[OT-RNP]) and ΔPosm over the period of salt loading for peptide-treated animals and control animals (39.5 ± 8.9, r = 0.89 vs. 23.4 ± 5.9, fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) indicated an increased responsiveness of OT neurones, but this difference was not significant (p < 0.1426). Higher plasma levels of OT were generated by administering the 10 nmol dose of OT, and the slopes of the relationship between Δ[OT-RNP] and ΔPosm for peptide-treated animals and control animals (13.9 ± 1.6, r = 0.96 vs. 23.4 ± 8.9 fmol∙mL−1∙mosmol−1∙kg−1, r = 0.93) suggested a decreased responsiveness of OT neurones, but again this difference was not significant (p < 0.1637). However, there was a significant difference in the rise in OT-RNP with plasma osmolality for rats receiving high versus low dose of peptide (p < 0.0475). Our data indicate that peripherally administered OT, unlike VP, does not exert a negative feedback influence on osmotically stimulated release from VP neurones and most probably OT neurones. However, it cannot be ruled out that the lack of modulation of magnocellular neurones by the high dose of OT could be due to the summation of a positive OT effect (since the 1-nmol group appeared to exhibit an enhancing effect) and of a negative VP effect as indicated by blood pressure increases and plasma dilution. OT also does not appear to have an influence on basal release from magnocellular neurones.Key words: neurophysins, oxytocin neurones, vasopressin neurones.


2014 ◽  
Vol 26 (4) ◽  
pp. 205-216 ◽  
Author(s):  
V. A. Tobin ◽  
G. Arechaga ◽  
P. J. Brunton ◽  
J. A. Russell ◽  
G. Leng ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document