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Query: UNIPROT:P01178 (
oxytocin
)
15,767
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The presence of corticotropin-releasing hormone (CRH) receptors type-1 (
CRHR
-1) and type-2 (
CRHR
-2alpha) in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, and the effects of i.c.v. injection of CRH and urocortin on arginine vasopressin (AVP) and
oxytocin
release, have suggested that CRH ligands have a role in osmoregulation. In this study, double labelling in situ hybridization using 35S-labelled
CRHR
-1 or
CRHR
-2alpha and digoxigenin-labelled AVP,
oxytocin
or CRH riboprobes was employed to examine the localization of
CRHR
-1 or
CRHR
-2alpha mRNA in the SON and PVN of control and osmotically stimulated rats. Rats received an i.p. hypertonic saline (1.5 M) injection or isotonic saline injection (controls), or 2% NaCl intake (salt loading) or tap water (controls) for 12 days. While
CRHR
-1 mRNA was undetectable in the SON and PVN in control rats, its expression was increased markedly at 4 h after i.p. hypertonic saline injection or after 12 days salt loading. Of the cells labelled with digoxigenin-AVP, 53% in the SON and 90% in the PVN coexpressed
CRHR
-1 mRNA after i.p. hypertonic saline injection. In oxytocinergic neurones, 73% in the SON and 91% in the PVN showed
CRHR
-1 autoradiographic grains higher than background levels after i.p. hypertonic saline injection. In addition, i.p. hypertonic saline induced
CRHR
-1 mRNA expression in digoxigenin-CRH stained cells in the parvocellular PVN.
CRHR
-2alpha transcripts were present in both the SON and PVN under basal conditions, and salt loading, but not acute i.p. hypertonic saline injection, further stimulated this expression. Double labelling in situ hybridization showed colocalization of
CRHR
-2alpha mRNA with AVP and
oxytocin
mRNA in the SON. These studies support a role for CRH and urocortin regulating the hypothalamo-neurohypophyseal system, and suggest a direct action of the peptides in the magnocellular neurones.
...
PMID:Vasopressin and oxytocin neurones of hypothalamic supraoptic and paraventricular nuclei co-express mRNA for Type-1 and Type-2 corticotropin-releasing hormone receptors. 1097 8
Maternal behavior and anxiety are potently modulated by the brain corticotropin-releasing factor (CRF) system postpartum. Downregulation of CRF in limbic brain regions is essential for appropriate maternal behavior and an adaptive anxiety response. Here, we focus our attention on arguably the most important brain region for maternal behavior, the hypothalamic medial preoptic area (MPOA). Within the MPOA, mRNA for CRF receptor subtype 1 (protein:
CRFR1
, gene: Crhr1) was more abundantly expressed than for subtype 2 (protein: CRFR2, gene: Crhr2), however expression of Crhr1, Crhr2 and CRF-binding protein (protein: CRFBP, gene: Crhbp) mRNA was similar between virgin and lactating rats. Subtype-specific activation of CRFR, predominantly
CRFR1
, in the MPOA decreased arched back nursing and total nursing under non-stress conditions. Following acute stressor exposure, only
CRFR1
inhibition rescued the stress-induced reduction in arched back nursing while
CRFR1
activation prolonged the decline in nursing. Furthermore, inhibition of
CRFR1
strongly increased maternal aggression in the maternal defense test.
CRFR1
activation had anxiogenic actions and reduced locomotion on the elevated plus-maze, however neither
CRFR1
nor R2 manipulation affected maternal motivation. In addition, activation of
CRFR1
, either centrally or locally in the MPOA, increased local
oxytocin
release. Finally, inhibition of CRFBP (a potent regulator of CRFR activity) in the MPOA did not affect any of the maternal parameters investigated. In conclusion, activity of CRFR in the MPOA, particularly of subtype 1, needs to be dampened during lactation to ensure appropriate maternal behavior. Furthermore,
oxytocin
release in the MPOA may provide a regulatory mechanism to counteract the negative impact of CRFR activation on maternal behavior.
...
PMID:Maternal stress and the MPOA: Activation of CRF receptor 1 impairs maternal behavior and triggers local oxytocin release in lactating rats. 2947
The neuropeptide
oxytocin
(OT) plays an important role in the regulation of social and anxiety-like behavior. Our previous studies have shown that OT neurons send projections from the hypothalamus to the dorsolateral bed nucleus of the stria terminalis (BNST
dl
), a forebrain region critically involved in the modulation of anxiety-like behavior. Importantly, these OT terminals in the BNST
dl
express presynaptic corticotropin releasing factor (CRF) receptor type 2 (CRFR2). This suggests that CRFR2 might be involved in the modulation of OT release. To test this hypothesis, we measured OT content in microdialysates collected from the BNST
dl
of freely-moving male Sprague-Dawley rats following the administration of a selective CRFR2 agonist (Urocortin 3) or antagonist (Astressin 2B, As2B). To determine if type 1 CRF receptors (
CRFR1
) are also involved, we used selective
CRFR1
antagonist (NBI35965) as well as CRF, a putative ligand of both
CRFR1
and CRFR2. All compounds were delivered directly into the BNST
dl
via reverse dialysis. OT content in the microdialysates was measured with highly sensitive and selective radioimmunoassay. Blocking CRFR2 with As2B caused an increase in OT content in BNST
dl
microdialysates, whereas CRFR2 activation by Urocortin 3 did not have an effect. The As2B-induced increase in OT release was blocked by application of the
CRFR1
antagonist demonstrating that the effect was dependent on
CRFR1
transmission. Interestingly, CRF alone caused a delayed increase in OT content in BNST
dl
microdialysates, which was dependent on CRF2 but not CRF1 receptors. Our results suggest that members of the CRF peptide family modulate OT release in the BNST
dl
via a fine-tuned mechanism that involves both
CRFR1
and CRFR2. Further exploration of mechanisms by which endogenous OT system is modulated by CRF peptide family is needed to better understand the role of these neuropeptides in the regulation of anxiety and the stress response.
...
PMID:Corticotropin-Releasing Factor Receptors Modulate Oxytocin Release in the Dorsolateral Bed Nucleus of the Stria Terminalis (BNST) in Male Rats. 2961 70