Oxytocin at physiological concentrations evokes adrenocorticotropin (ACTH) release from corticotrophs by increasing intracellular free calcium mobilized mainly from intracellular stores. Oxytocin displays synergistic or additive effects on ACTH-releasing factor or arginine vasopressin-induced ACTH secretion, respectively

Link, H.

doi:10.1210/en.130.4.2183

Cited by 27 publications

(21 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The maximal inhibition rates calculated from these data (70 -80% for astressin, 40 -50% for dPTyVP) definitely indicate that CRF dominantly mediates ACTH-secreting signals in the downstream cascade of central Y 5 activation. A lesser degree of inhibition shown in the treatment with dPTyVP might reflect the involvement of not only AVP but also oxytocin released into the hypophysial portal circulation, provided that dPTyVP is also an antagonist of oxytocin receptor (24), and this hormone may function as a hypophysiotropic factor (25). Surprisingly, we found no differences between the treatment with astressin alone and astressin plus dPTyVP in the maximal suppression of hPP-induced increases in ACTH and CORT (Fig.…”

Section: Discussionmentioning

confidence: 62%

Direct Evidence that Stimulation of Neuropeptide Y Y5 Receptor Activates Hypothalamo-Pituitary-Adrenal Axis in Conscious Rats via both Corticotropin-Releasing Factor- and Arginine Vasopressin-Dependent Pathway

Kakui

Kitamura

2007

Endocrinology

View full text Add to dashboard Cite

An abundance of data suggests a crucial role of neuropeptide Y (NPY) as an activator of the hypothamamo-pituitary-adrenal (HPA) axis. However, there is quite limited evidence regarding receptors that mediate this response. Here, we address the possibility that Y(5) receptor subtype may be responsible for NPY-induced activation of HPA axis. For this purpose, the effects of an intracerebroventricular injection of Y(5)-selective agonist, [cPP(1-7), NPY(19-23), Ala(31), Aib(32), Gln(34)]-human pancreatic polypeptide (hPP), on circulating ACTH and corticosterone in conscious rats were evaluated. Central injection of hPP (100 pmol) produced significant increases in plasma ACTH and corticosterone compared with artificial cerebrospinal fluid, and previous treatment with a novel Y(5)-selective antagonist, FMS586 [3-(9-isopropyl-6,7,8,9-tetrahydro-5H-carbazol-3-yl)-1-methyl-1-(2-pyridin-4-yl-ethyl)-urea hydrochloride] (25 mg/kg, po), completely blocked these alterations. Pretreatment with corticotropin-releasing factor (CRF) receptor antagonist (astressin, 10-50 microg/rat, iv) or arginine vasopressin (AVP) receptor antagonist ([deamino-Pen(1), O-Me-Tyr(2), Arg(8)] vasopressin; 3-30 microg/rat, iv) differentially suppressed these increases by 70-80 or 40-50%, respectively. The combined treatment showed no additive effect of these antagonists. Furthermore, an exogenous AVP (0.3 microg/rat, iv)-induced HPA activation was fully inhibited by astressin, suggesting a convergent pathway of AVP receptor signals onto CRF neurons. Central injection of hPP also evoked marked up-regulation of mRNA expression for CRF and AVP in the hypothalamus, which, likewise, were completely reversed by FMS586. Our observations provide the first evidence that selective stimulation of Y(5) receptor provokes activation of the HPA axis and its downstream pathway is chiefly composed of both CRF (primary regulator) and AVP (subordinate to the former) with distinct relative contribution.

show abstract

Section: Discussionmentioning

confidence: 62%

Direct Evidence that Stimulation of Neuropeptide Y Y5 Receptor Activates Hypothalamo-Pituitary-Adrenal Axis in Conscious Rats via both Corticotropin-Releasing Factor- and Arginine Vasopressin-Dependent Pathway

Kakui

Kitamura

2007

Endocrinology

View full text Add to dashboard Cite

show abstract

“…Oxt was originally thought to have an agonistic effect on adrenocorticotropin hormone (ACTH) release and a facilitative effect on corticotropin-releasing factor (CRF)-mediated ACTH release at the level of the pituitary: Oxt administered to superfused hemipituitaries or pituitary cells in vitro causes the release of ACTH (Link et al , 1992) and potentiates ACTH release in response to CRF (Antoni et al , 1983; Gibbs et al , 1984; Link et al , 1992). This potentiation of ACTH release is due to Oxt’s action at the Avpr1b receptor in the pituitary (Schlosser et al , 1994).…”

Section: Behaviormentioning

confidence: 99%

Oxytocin: The Great Facilitator of Life

Lee

Macbeth

Pagani

et al. 2009

Progress in Neurobiology

642

634

View full text Add to dashboard Cite

Oxytocin (Oxt) is a nonapeptide hormone best known for its role in lactation and parturition. Since 1906 when its uterine-contracting properties were described until 50 years later when its sequence was elucidated, research focused on its peripheral roles in reproduction. Only over the past several decades have researchers focused on what functions Oxt might have in the brain, the subject of this review. Immunohistochemical studies revealed that magnocellular neurons of the hypothalamic paraventricular and supraoptic nuclei are the neurons of origin for the Oxt released from the posterior pituitary. Smaller cells in various parts of the brain, as well as release from magnocellular dendrites, provide the Oxt responsible for modulating various behaviors at its only identified receptor. Although Oxt is implicated in a variety of “non-social” behaviors, such as learning, anxiety, feeding and pain perception, it is Oxt’s roles in various social behaviors that have come to the fore recently. Oxt is important for social memory and attachment, sexual and maternal behavior, and aggression. Recent work implicates Oxt in human bonding and trust as well. Human disorders characterized by aberrant social interactions, such as autism and schizophrenia, may also involve Oxt expression. Many, if not most, of Oxt’s functions, from social interactions (affiliation, aggression) and sexual behavior to eventual parturition, lactation and maternal behavior, may be viewed as specifically facilitating

show abstract

“…PLC-␤ activation results in the generation of inositol 1,4,5-trisphosphate and 1,2-diacylglycerol; the former triggers the release of Ca 2ϩ from the endoplasmic reticulum and the latter stimulates protein kinase C. The G q/11 -PLC-Ca 2ϩ mobilization pathway is likely operative in this gland as OT-induced Ca 2ϩ mobilization was observed in a gonadotroph cell line (45), corticotrophs (46,47), and lactotrophs (12,13). Here we establish that OT can evoke transients of [Ca 2ϩ ] i in primary cultured gonadotrophs and somatotrophs and further show that the pattern of [Ca 2ϩ ] i dynamics stimulated by OT is cell type specific, perhaps most strikingly demonstrated by the oscillations seen in gonadotrophs.…”

Section: Discussionmentioning

confidence: 94%

“…Given that OT can also act in corticotrophs (38,44) to modulate ACTH release (47,63) and may have an inhibitory effect on thyrotrophs (64), the nonapeptide may modulate anterior pituitary hormone release through direct actions on possibly all endocrine cell types of the gland.…”

Section: Discussionmentioning

confidence: 99%

Direct Stimulatory Effects of Oxytocin in Female Rat Gonadotrophs and Somatotrophs In Vitro: Comparison With Lactotrophs

et al. 2014

View full text Add to dashboard Cite

The peptide oxytocin (OT) is secreted by hypothalamic neurons and exerts numerous actions related to reproduction. OT stimulation of prolactin secretion in female rats is important during the estrous cycle, pregnancy, and lactation. Here we report that OT also stimulates transients of intracellular Ca(2+) concentration in somatotrophs and gonadotrophs as well as the release of GH and LH in a dose-dependent manner with EC50 values that closely correspond to the ligand affinity of the OT receptor (OTR). Remarkably, the hormone-releasing effect of OT in these two cell types is 2 orders of magnitude more sensitive than that in lactotrophs. The specific OTR agonist [Thr(4),Gly(7)]-oxytocin acutely stimulated the release of LH, GH, and prolactin from female rat pituitary cells in primary culture and increased intracellular Ca(2+) concentration in gonadotrophs, somatotrophs, and lactotrophs. In these three cell types, the effects on hormone release and intracellular Ca(2+) of both OT and [Thr(4),Gly(7)]oxytocin were abolished by the specific OT receptor antagonist desGly-NH2-d(CH2)5[D-Tyr(2),Thr(4)]OVT but not by the highly selective vasopressin V1a receptor antagonist, d(CH2)5[Tyr(Me)(2),Dab(5)]AVP. Furthermore, 10 nM arginine vasopressin stimulated LH and GH release comparably with a dose of OT that was at least 10 times lower. Finally, the presence of the OTR-like immunoreactivity could be observed in all three cell types. Taken together, these results show that OT directly stimulates gonadotrophs, somatotrophs, and lactotrophs through OT receptors and suggest that OT signaling may serve to coordinate the release of different pituitary hormones during specific physiological conditions.

show abstract

Cited by 27 publications

References 25 publications

Direct Evidence that Stimulation of Neuropeptide Y Y5 Receptor Activates Hypothalamo-Pituitary-Adrenal Axis in Conscious Rats via both Corticotropin-Releasing Factor- and Arginine Vasopressin-Dependent Pathway

Direct Evidence that Stimulation of Neuropeptide Y Y5 Receptor Activates Hypothalamo-Pituitary-Adrenal Axis in Conscious Rats via both Corticotropin-Releasing Factor- and Arginine Vasopressin-Dependent Pathway

Oxytocin: The Great Facilitator of Life

Direct Stimulatory Effects of Oxytocin in Female Rat Gonadotrophs and Somatotrophs In Vitro: Comparison With Lactotrophs

Contact Info

Product

Resources

About