Release of oxytocin and vasopressin by magnocellular nuclei in vitro: specific facilitatory effect of oxytocin on its own release

1984 ◽  
Vol 102 (1) ◽  
pp. 63-NP ◽  
Author(s):  
F. Moos ◽  
M. J. Freund-Mercier ◽  
Y. Guerné ◽  
J. M. Guerné ◽  
M. E. Stoeckel ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Male Rats ◽  
Facilitatory Effect ◽  
Vasopressin Release ◽  
Paraventricular Nuclei ◽  
Magnocellular Nuclei ◽  
Oxytocin Release ◽  
Supraoptic Nuclei

ABSTRACT The release of endogenous oxytocin and vasopressin by rat paraventricular and supraoptic nuclei in vitro during a 10-min period, 30 min after beginning the incubation, was measured radioimmunologically. Mean basal hormone release per 10 min and per pair of nuclei was: 128·4 ± 12·4 (s.e.m.) pg vasopressin (n = 15) and 39·0 ± 3·0 pg oxytocin (n = 66) for supraoptic nuclei from male rats; 273·9 ± 42·6 pg vasopressin (n = 11) and 34·2 ± 3·5 pg oxytocin (n = 15) for supraoptic nuclei from lactating rats; 70·0 ± 8·6 pg vasopressin (n = 52) and 21·8 ± 1·3 pg oxytocin (n = 68) for paraventricular nuclei from male rats; 59·1 ± 8·6 pg vasopressin (n = 10) and 27·0 ± 4·6 pg oxytocin (n = 16) for paraventricular nuclei from lactating rats. In male and lactating rats, both nuclei contained and released more vasopressin than oxytocin. For oxytocin alone, the paraventricular nucleus of male rats contained and released significantly less hormone than the supraoptic nucleus. This difference was not apparent in lactating rats. For vasopressin alone, the paraventricular nucleus contained and released significantly less hormone than the supraoptic nucleus in both male and lactating rats. When the hormone released was calculated as a percentage of the total tissue content the release was about 0·9% for oxytocin from both nuclei in male and lactating rats and also for vasopressin in lactating rats, but was only about 0·5% for vasopressin from both nuclei in male rats. The influence of oxytocin and analogues of oxytocin (including one antagonist) upon the release of oxytocin and vasopressin was studied. Adding oxytocin to the incubation medium (0·4–4 nmol/l solution) induced a dose-dependent rise in oxytocin release from both nuclei of male or lactating rats. A 4 nmol/l solution of isotocin had a similar effect to a 0·4 nmol/l solution of oxytocin, but arginine-vasopressin never affected basal release of oxytocin. In no case was vasopressin release modified. An oxytocin antagonist (1 μmol/l solution) significantly reduced basal oxytocin release and blocked the stimulatory effect normally induced by exogenous oxytocin, as did gallopamil hydrochloride (D600, 10 μmol/l solution), a Ca2+ channel blocker, or incubation in a Ca2+-free medium. These findings are discussed in relation to the literature on the central effects of neurohypophysial peptides. It may be concluded that the regulatory role of endogenous oxytocin in the hypothalamus on the milk-ejection reflex could result from its local release in the extracellular spaces of magnocellular nuclei. J. Endocr. (1984) 102, 63–72

Corticotrophin-releasing peptides in rat hypophysial portal blood after paraventricular lesions: a marked reduction in the concentration of corticotrophin-releasing factor-41, but no change in vasopressin

1990 ◽  
Vol 125 (2) ◽  
pp. 175-183 ◽  
Author(s):  
F. A. Antoni ◽  
G. Fink ◽  
W. J. Sheward
Keyword(s):  
Median Eminence ◽  
Feedback Inhibition ◽  
Portal Blood ◽  
Corticotrophin Releasing Factor ◽  
Paraventricular Nuclei ◽  
Oxytocin Release ◽  
Male Wistar Rats ◽  
Hypophysial Portal ◽  
Supraoptic Nuclei

ABSTRACT Previous data show that corticotrophin-releasing factor-41 (CRF-41), arginine vasopressin (AVP) and oxytocin are released into hypophysial portal blood. It has been presumed that the CRF-41 originates mainly from parvicellular neurones of the paraventricular nuclei (PVN); however, AVP and oxytocin could also be derived as a consequence of preterminal release from magnocellular projections to the neurohypophysis. The latter has been suggested to be the case for AVP as assessed by studies of the median eminence in vitro. Here we have investigated the source of CRF-41, AVP and oxytocin in hypophysial portal blood of adult male Wistar rats 8–10 days after surgical lesioning of the PVN. In PVN-lesioned animals the output of CRF-41 into hypophysial portal blood was reduced by about 90%, and that of oxytocin by about 40%: however, the output of AVP into portal blood was reduced only by about 10%. The release of AVP into portal blood increased after adrenalectomy; this increased release could be returned to normal by treatment with dexamethasone. No change of AVP release occurred after adrenalectomy in animals in which the PVN had been lesioned. These results show (i) that most of the CRF-41 released into hypophysial portal blood is derived from the PVN, (ii) that in PVN-lesioned animals AVP and oxytocin release remains at near normal or 60% of normal respectively, suggesting that a substantial amount of both neuropeptides in portal blood is derived as a consequence of preterminal release from supraoptic nuclei projections in the median eminence, and (iii) that glucocorticoid feedback inhibition of AVP release is exerted at the level of the PVN. Journal of Endocrinology (1990) 125, 175–183

Oxytocin actions within the supraoptic and paraventricular nuclei: differential effects on peripheral and intranuclear vasopressin release

2006 ◽  
Vol 291 (1) ◽  
pp. R29-R36 ◽  
Author(s):  
Inga D. Neumann ◽  
Luz Torner ◽  
Nicola Toschi ◽  
Alexa H. Veenema
Keyword(s):  
Supraoptic Nucleus ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Elevated Plasma ◽  
Acth Secretion ◽  
Vasopressin Release ◽  
Paraventricular Nuclei ◽  
Pituitary Adrenal Axis

In response to forced swimming (FS), AVP is released somato-dendritically within the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but not from neurohypophyseal terminals into blood. Together with AVP, oxytocin (OXT) is released within the SON and PVN. Here, we studied the role of intra-SON and intra-PVN OXT in the regulation of local AVP release and into the blood in male rats. Within the SON, bilateral retrodialysis of an OXT receptor antagonist (OXT-A) increased local AVP release in response to FS [60 s, 21°C, vehicle twofold, not significant (ns); OXT-A: 15-fold increase, P < 0.05] without significantly affecting basal AVP release. In addition, local OXT-A elevated plasma AVP secretion under basal conditions (twofold increase, P < 0.05) without further elevation after FS. Within the PVN, exposure to FS elevated local AVP release, reaching significance only in the OXT-A group (vehicle: 1.4-fold, ns; OXT-A: 1.6-fold increase, P = 0.050). Bilateral OXT-A into the PVN did not affect peripheral AVP secretion either under basal or stress conditions. Basal ACTH concentrations tended to be elevated by local OXT-A within the PVN (1.7-fold increase, P = 0.076). In contrast, the swim-induced ACTH secretion was attenuated after retrodialysis of OXT-A within both the SON (at 5 min) and PVN (at 15 min) ( P < 0.05 both) compared with vehicle. The results demonstrate a receptor-mediated effect of OXT within the SON and PVN on local and neurohypophyseal AVP release, which depends upon the activity conditions. Further, while exerting an inhibitory effect on hypothalamo-pituitary-adrenal axis activity under basal conditions, hypothalamic OXT is essential for an adequate acute ACTH response.

scholarly journals Stimulus-secretion coupling in the neurohypophysis of the jerboa Jaculus orientalis.

1994 ◽  
Vol 195 (1) ◽  
pp. 19-34
Author(s):  
A Raji ◽  
J J Nordmann
Keyword(s):  
Time Course ◽  
Physiological State ◽  
Nerve Endings ◽  
Neurosecretory System ◽  
Channel Blockers ◽  
Vasopressin Release ◽  
Oxytocin Release ◽  
Stimulus Secretion Coupling ◽  
Stimulation Of

1. In many mammals, severe dehydration is known to cause exhaustion of the vasopressin content of the neural lobe. Here, we have examined the physiological state of the neurohypophysis of the jerboa Jaculus orientalis, a rodent inhabitant of a semi-desert climate. 2. Isolated neurohypophyses and neurosecretory nerve endings were perfused in vitro and vasopressin and oxytocin release were determined by radioimmunoassay. 3. Electrical stimulation of the neurohypophysis with bursts of pulses mimicking the activity of hypersecreting neuroendocrine neurones induced similar increases of secretion in both control animals and animals dehydrated for up to 2 months. Neurohormone release was greatly potentiated when the bursts of pulses were separated by silent intervals. 4. Prolonged stimulation of neurohypophyses from both control and dehydrated animals induced a sustained increase of vasopressin release; in contrast, oxytocin release under similar conditions showed a biphasic secretory pattern consisting of a transient increase that subsequently decreased to a steady level whose amplitude was similar to that for vasopressin. 5. K(+)-induced secretion was largely inhibited by the Ca2+ channel blockers nicardipine and omega-conotoxin, suggesting that in this neurosecretory system both L- and N-type calcium channels play a major role in stimulus-secretion coupling. Depolarization of isolated nerve endings using a fast-flow perifusion system showed that there was no difference in the amplitude and the time course of the secretory response in dehydrated and hydrated animals. 6. The results demonstrate that, despite the climatic conditions in which the jerboas live, their neural lobes retain the capacity to release, upon depolarization of the plasma membrane of the nerve endings, large amounts of neurohormone. It is concluded that the neurohypophyseal peptidergic release system in the dehydrated jerboa functions adequately even under extreme environmental stress.

Stimuli and consequences of dendritic release of oxytocin within the brain

2007 ◽  
Vol 35 (5) ◽  
pp. 1252-1257 ◽  
Author(s):  
I.D. Neumann
Keyword(s):  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Supraoptic Nucleus ◽  
Brain Regions ◽  
Model System ◽  
Intracerebral Microdialysis ◽  
Psychotherapeutic Intervention ◽  
Psychiatric Illnesses ◽  
Oxytocin Release ◽  
The Brain

The brain oxytocin system has served as a distinguished model system in neuroendocrinology to study detailed mechanisms of intracerebral release, in particular of somatodendritic release, and its behavioural and neuroendocrine consequences. It has been shown that oxytocin is released within various brain regions, but evidence for dendritic release is limited to the main sites of oxytocin synthesis, i.e. the hypothalamic SON (supraoptic nucleus) and PVN (paraventricular nucleus). In the present paper, stimuli of dendritic release of oxytocin and the related neuropeptide vasopressin are discussed, including parturition and suckling, i.e. the period of a highly activated brain oxytocin system. Also, exposure to various pharmacological, psychological or physical stressors triggers dendritic oxytocin release, as monitored by intracerebral microdialysis within the SON and PVN during ongoing behavioural testing. So far, dendritic release of the neuropeptide has only been demonstrated within the hypothalamus, but intracerebral oxytocin release has also been found within the central amygdala and the septum in response to various stimuli including stressor exposure. Such a locally released oxytocin modulates physiological and behavioural reproductive functions, emotionality and hormonal stress responses, as it exerts, for example, pro-social, anxiolytic and antistress actions within restricted brain regions. These discoveries make oxytocin a promising neuromodulator of the brain for psychotherapeutic intervention and treatment of numerous psychiatric illnesses, for example, anxiety-related diseases, social phobia, autism and postpartum depression.

scholarly journals Nesfatin-1 Neurons in Paraventricular and Supraoptic Nuclei of the Rat Hypothalamus Coexpress Oxytocin and Vasopressin and Are Activated by Refeeding

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1295-1301 ◽  
Author(s):  
Daisuke Kohno ◽  
Masanori Nakata ◽  
Yuko Maejima ◽  
Hiroyuki Shimizu ◽  
Udval Sedbazar ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Mrna Expression ◽  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Energy Homeostasis ◽  
Rat Hypothalamus ◽  
Hypothalamic Nuclei ◽  
Vasopressin Neurons ◽  
Fine Localization ◽  
Supraoptic Nuclei

Nesfatin-1, a newly discovered satiety molecule, is located in the hypothalamic nuclei, including the paraventricular nucleus (PVN) and supraoptic nucleus (SON). In this study, fine localization and regulation of nesfatin-1 neurons in the PVN and SON were investigated by immunohistochemistry of neuropeptides and c-Fos. In the PVN, 24% of nesfatin-1 neurons overlapped with oxytocin, 18% with vasopressin, 13% with CRH, and 12% with TRH neurons. In the SON, 35% of nesfatin-1 neurons overlapped with oxytocin and 28% with vasopressin. After a 48-h fast, refeeding for 2 h dramatically increased the number of nesfatin-1 neurons expressing c-Fos immunoreactivity by approximately 10 times in the PVN and 30 times in the SON, compared with the fasting controls. In the SON, refeeding also significantly increased the number of nesfatin-1-immunoreactive neurons and NUCB2 mRNA expression, compared with fasting. These results indicate that nesfatin-1 neurons in the PVN and SON highly overlap with oxytocin and vasopressin neurons and that they are activated markedly by refeeding. Feeding-activated nesfatin-1 neurons in the PVN and SON could play a role in the postprandial regulation of feeding behavior and energy homeostasis.

Endogenous opioid control of somatodendritic oxytocin release from the hypothalamic supraoptic and paraventricular nuclei in vitro

1996 ◽  
Vol 25 (1) ◽  
pp. 17-24 ◽  
Author(s):  
C.D. Ingram ◽  
V. Kavadas ◽  
M.R.M. Thomas ◽  
J.D. Threapleton
Keyword(s):  
Endogenous Opioid ◽  
Paraventricular Nuclei ◽  
Oxytocin Release

Inhibitory effects of endothelin-3 on vasopressin release from rat supraoptic nucleus in vitro

1992 ◽  
Vol 141 (2) ◽  
pp. 147-150 ◽  
Author(s):  
Shigeki Yamamoto ◽  
Isao Morimoto ◽  
Hiroshi Yamashita ◽  
Sumiya Eto
Keyword(s):  
Supraoptic Nucleus ◽  
Inhibitory Effects ◽  
Vasopressin Release ◽  
Endothelin 3

scholarly journals Muscarinic M2 receptor promotes vasopressin synthesis in mice supraoptic nuclei

2018 ◽  
Vol 237 (2) ◽  
pp. 207-216
Author(s):  
Hiroshi Nagano ◽  
Yuki Sobue ◽  
Hayato Matsuyama ◽  
Shoichiro Saito ◽  
Hiroki Sakai ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Knockout Mice ◽  
Receptor Expression ◽  
Muscarinic Agonist ◽  
Wild Type ◽  
Vasopressin Release ◽  
Paraventricular Nuclei ◽  
Vasopressin Secretion ◽  
Vasopressin Synthesis ◽  
Supraoptic Nuclei

Muscarinic acetylcholine receptors have been suggested to be implicated in arginine–vasopressin secretion because intracerebroventricular muscarinic agonist administration induces arginine–vasopressin release into the circulation. Although which subtype is involved in the regulation of arginine–vasopressin secretion is unclear, M2 receptors have been reported to be highly expressed in the hypothalamus. In the present study, M2 receptor-knockout mice were used to elucidate whether M2 receptor regulates arginine–vasopressin synthesis in the paraventricular nuclei and supraoptic nuclei of the hypothalamus. The number of arginine–vasopressin-immunoreactive neurons in M2 receptor-knockout mice was significantly decreased in the supraoptic nuclei, but not in the paraventricular nuclei compared with wild-type mice. Plasma arginine–vasopressin level in M2 receptor-knockout mice was also significantly lower than in the wild-type mice. Urinary volume and frequency as well as water intake in M2 receptor-knockout mice were significantly higher than those in wild-type mice. The V2 vasopressin receptor expression in kidneys of M2 receptor-knockout mice was comparable with that of wild-type mice, and increased urination in M2 receptor-knockout mice was significantly decreased by administration of desmopressin, a specific V2 receptor agonist, suggesting that V2 receptors in the kidneys of M2 receptor-knockout mice are intact. These results suggest that M2 receptors promote arginine–vasopressin synthesis in the supraoptic nuclei and play a role in the regulation and maintenance of body fluid.

Characterization of hypothalamic noradrenaline receptors in the supraoptic nucleus and periventricular region of the paraventricular nucleus of mice in vitro

1986 ◽  
Vol 369 (1-2) ◽  
pp. 37-47 ◽  
Author(s):  
Kiyotoshi Inenaga ◽  
Richard E.J. Dyball ◽  
Shiguru Okuya ◽  
Hiroshi Yamashita
Keyword(s):  
Paraventricular Nucleus ◽  
Supraoptic Nucleus
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