Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropeptide B (NPB) was identified to be an endogenous, peptide ligand for the orphan receptors GPR7 and GPR8. Because GPR7 is expressed in rat brain and, in particular, in the hypothalamus, we hypothesized that NPB might interact with neuroendocrine systems that control hormone release from the anterior pituitary gland. No significant effects of NPB were observed on the in vitro releases of prolactin, adrenocorticotropic hormone (ACTH) or growth hormone (GH) when log molar concentrations ranging from 1 pM to 100 nM NPB were incubated with dispersed anterior pituitary cells harvested from male rats. In addition NPB (100 nM) did not alter the concentration response stimulation of prolactin secretion by thyrotropin-releasing hormone, ACTH secretion by corticotropin-releasing factor (CRF) and GH secretion by GH-releasing hormone. However, NPB, when injected into the lateral cerebroventricle (i.c.v.) of conscious, unrestrained male rats, elevated prolactin and corticosterone, and lowered GH levels in circulation. The threshold dose for the effect on corticosterone and prolactin levels was 1.0 nmol, while that for the effect on GH release was 3.0 nmol NPB. Pretreatment with a polyclonal anti-CRF antiserum completely blocked the ability of NPB to stimulate ACTH release and significantly inhibited the effect of NPB on plasma corticosterone levels. NPB administration i.c.v. did not significantly alter plasma vasopressin and oxytocin levels in conscious rats. It did stimulate feeding (minimum effective dose 1.0 nmol) in sated animals in a manner similar to that of the other endogenous ligand for GPR7, neuropeptide W. We conclude that NPB can act in the brain to modulate neuroendocrine signals accessing the anterior pituitary gland, but does not itself act as a releasing or inhibiting factor in the gland, at least with regard to prolactin, ACTH and GH secretion.
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PMID:Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats. 1550 May 44

Neuropeptide B (NPB) is a recently identified endogenous ligand for the orphan G protein-coupled receptors GPR7 and GPR8. NPB mRNA is expressed in the human, rat, and mouse brain. With the use of an antiserum directed against the rat NPB, immunoreactivity to NPB (irNPB) was detected in several discrete areas of the hypothalamus and midbrain. In the hypothalamus, irNPB cells were present in the medial preoptic area and nucleus, ventromedial preoptic nucleus, retrochiasmatic nucleus, paraventricular hypothalamic nucleus, supraoptic nucleus, accessory neurosecretory nuclei, periventricular hypothalamic nucleus, dorsomedial hypothalamic nucleus, supraoptic retrochiasmatic nucleus, lateral hypothalamic area, posterior hypothalamic area, dorsal hypothalamic area, and zona incerta. A few irNPB perikarya were noted in the arcuate nucleus, whereas a dense network of nerve fibers was present in the median eminence. In the midbrain, irNPB somata were noted in the substantia nigra (compact, reticular, medial, and lateral parts), paranigral nucleus, ventral tegmental area, interfascicular nucleus, and dorsal raphe nucleus. Neurons in the Edinger-Westphal were strongly labeled. Labeled cells were not detected in the cortex, medulla oblongata, and spinal cord; few lightly labeled cells were occasionally seen in the hippocampus. Double labeling the hypothalamic sections with NPB antiserum and vasopressin or oxytocin antibody revealed that a population of vasopressin- but not oxytocin-immunoreactive cells was irNPB. Tyrosine hydroxylase-positive neurons in the midbrain, presumably dopaminergic, were irNPB. The distribution of irNPB neurons in several areas of the hypothalamus and midbrain together with the colocalization with vasopressin or tyrosine hydroxylase suggests that the peptide may subserve neuroendocrine, autonomic, and motor functions.
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PMID:Neuropeptide B immunoreactivity in the central nervous system of the rat. 1591 Jul 74

The administration of the neuropeptide W (NPW) and neuropeptide B (NPB) in rodents has been shown to influence the activity of a variety of autonomic and neuroendocrine systems. The paraventricular nucleus (PVN) is a major autonomic and neuroendocrine integration site in the hypothalamus, and neurones within this nucleus express the receptor for these ligands, NPB/W receptor 1 (NPBWR1). In the present study, we used whole cell patch clamp recordings coupled with single-cell reverse transcriptase-polymerase chain reaction to examine the effects of neuropeptide W-23 (NPW-23) on the excitability of identified PVN neurones. Oxytocin, vasopressin and thyrotrophin-releasing hormone neurones were all found to be responsive to 10 nm NPW-23, although both depolarising and hyperpolarising effects were observed in each of these cell groups. By contrast, corticotrophin-releasing hormone cells were unaffected. Further subdivision of chemically phenotyped cell groups into magnocellular, neuroendocrine or pre-autonomic neurones, using their electrophysiological fingerprints, revealed that neurones projecting to medullary and spinal targets were predominantly inhibited by NPW-23, whereas those that projected to median eminence or neural lobe showed almost equivalent numbers of depolarising and hyperpolarising cells. The demonstration of particular phenotypic populations of PVN neurones showing NPW-induced effects on excitability reinforces the importance of the NPB/NPW neuropeptide system as a regulator of autonomic function.
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PMID:Neuropeptide W has cell phenotype-specific effects on the excitability of different subpopulations of paraventricular nucleus neurones. 1968 47