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)

Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS). Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival. Axotomy induces transient (1-21 d) upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin II, and neuropeptide Y. These neuropeptides are colocalized with "classic" neurotransmitters (acetylcholine, aspartate, glutamate) or neurohormones (vasopressin, oxytocin) that are downregulated by axotomy in the same neuronal cells. It is more likely that neuronal cells, in response to axotomy, increase expression of neuropeptides that promote their survival and regeneration, and may downregulate substances related to their transmitter or secretory activities.
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PMID:Neuropeptide messenger plasticity in the CNS neurons following axotomy. 757 12

At the neurosecretory terminals in the neural lobe, oxytocin secretion is restrained by co-secreted endogenous opioids, which act via kappa-receptors. The co-secreted opioids include products of pro-dynorphin (released by both vasopressin and oxytocin terminals) and proenkephalin (released by oxytocin terminals). In morphine-tolerant rats this opioid mechanism is more effective, but in late pregnancy it is less effective. Opioids also act directly on oxytocin cell bodies, via separate mu- and kappa-receptors, inhibiting excitation by all stimuli tested, and also exert presynaptic and more distal actions on afferent systems. During chronic morphine exposure, tolerance and dependence develop in oxytocin neurones; the former involves reduction in mu-opioid receptor density, while the latter may involve compensatory upregulation of mechanisms regulating Ca2+ influx. In mid-pregnancy, the effectiveness of opioid mechanisms in the neural lobe increases, assisting the accumulation of oxytocin stores in advance of parturition, but by the end of pregnancy the effectiveness of these mechanisms is reduced. At this time, a separate endogenous opioid system, acting via mu-receptors, actively restrains the electrical activity of oxytocin neurones. Release of this endogenous opioid inhibition may contribute to the increase in activity during parturition analogous to that occurring during morphine withdrawal excitation. Central opioid mechanisms retain the ability to control oxytocin neurones during parturition, and can interrupt established parturition by inhibiting oxytocin neurone firing rate in disadvantageous environmental circumstances.
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PMID:Opioid tolerance and dependence in the magnocellular oxytocin system: a physiological mechanism? 764 4

Ample evidence indicates that in nerve cells, several individual proteins are locally synthesized in postsynaptic domains in dendrites. By contrast, axonal terminals, at least in mammals, are generally thought to lack protein synthetic capacity. However, axonal nerve endings of the hypothalamo-neurohypophyseal tract have recently been shown to contain mRNAs encoding vasopressin, oxytocin, dynorphin, and neurofilament. In this report, we identify BC1 RNA, a small RNA polymerase III transcript that is specifically expressed in neurons, in hypothalamo-neurohypophyseal axons. BC1 RNA has previously been shown to be located in somatic and dendritic domains of various types of neurons in the rat nervous system. Here we present evidence to show that BC 1 RNA, like several neuropeptide mRNAs, is axonally transported from magnocellular hypothalamic neurons to neurosecretory nerve endings in the posterior pituitary. BC1 RNA, which has been reported to be a component of a ribonucleoprotein particle, is thus colocalized with dendritic mRNAs in dendritic domains and with axonal mRNAs in axonal domains, respectively. Such colocalization is indicative of functional interactions of BC1 RNA with those mRNAs that are targeted to extrasomatic domains of nerve cells.
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PMID:Transport of BC1 RNA in hypothalamo-neurohypophyseal axons. 769 10

Endogenous opioid peptides derived from all three opioid precursors have been isolated from the pituitary of mammalian species. While beta-endorphin of the anterior lobe was soon shown to be secreted into the circulation as a hormone, the dynorphins and the enkephalins were found to occur in relative small quantities too low for export and effects in the periphery. With respect to the prodynorphin family in the neural lobe convincing evidence has been accumulated for a role of dynorphin A(1-8) in the local control of the release of the hormone oxytocin. The function of the enkephalins in the anterior and neural lobes, in spite of many efforts with in situ hybridization, immunocytochemistry, receptor autoradiography and receptor binding and bioassays, is still elusive. Research should be directed into the role of enkephalins in different physiological states, developmental stages and in non-mammalian vertebrate species.
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PMID:Opioid peptides in the pituitary: a hormone, a paracrine modulator and a peptide in search of a function. 769 35

The secretion of oxytocin (OXT) from the neurohypophysis is modulated by the actions of opioids acting via kappa-receptors. The vasopressin (AVP)-containing nerve terminals in the neurohypophysis contain the kappa-opioid agonist dynorphin, but endogenous opioid restraint of OXT secretion is observed even when AVP release is not activated, suggesting that another source of opioids is responsible for modulating OXT secretion. We now report that acute stimulation of the rat neural lobe in vivo results in depletion of the neural lobe content of OXT, AVP, dynorphin A1-17, dynorphin A1-8 and metenkephalin (Met-Enk). The dynorphin content is depleted to a similar extent as that of OXT and AVP; a correlation analysis suggests that while most dynorphin is co-secreted with AVP, a significant portion is co-secreted with OXT, consistent with a co-localisation of dynorphin with OXT. Met-Enk was depleted to a lesser extent than either hormone, consistent with a partial localisation in non-releasable pools. However, depletion of Met-Enk was also observed following naloxone-precipitated opioid withdrawal accompanying selective hypersecretion of OXT, suggesting co-secretion of OXT and Met-Enk. Met-Enk is a mu-opioid receptor agonist, but extended forms of Met-Enk, as we now report, are active at neurohypophysial kappa-receptors.
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PMID:Stimulus-induced depletion of pro-enkephalins, oxytocin and vasopressin and pro-enkephalin interaction with posterior pituitary hormone release in vitro. 770 Apr 99

Regulation of oxytocin release from spinal cord synaptosomes was investigated using in vitro preparations. Experiments were designed to determine whether opioid peptides regulate oxytocin release from spinal cord synaptosomes, as they do from synaptosomes derived from neurohypophysis. Oxytocin release was evoked by the addition of 56 mM KCl in synaptosomes prepared from thoracic and lumbosacral parts of the spinal cord. Addition of 5 microM naloxone, 1 min prior to the addition of the stimulus, caused a significant (p < 0.025) increase of oxytocin release. Prior addition of 5 microM dynorphin, demonstrated a significant (p < 0.01) decrease whereas addition of 5 microM [D-Ala2,N-Me-Phe4,Gly-ol]-enkephalin showed no effect on KCl-induced OT release. The results suggest that spinal cord OT release is under inhibitory control of opioid peptides and the opioids act via the kappa opioid receptor.
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PMID:Opioid modulation of oxytocin release from spinal cord synaptosomes. 782 43

Dynamic changes of contents of beta-endorphin, leu-enkephalin and oxytocin in plasma were determined in seventeen fracture patients with shock, fascial space syndromes, or infection postoperation. There was significant rise of contents in beta-endorphin and leu-enkephalin but not in oxytocin after trauma, Of those accompanied by infection postoperation, beta-endorphin and oxytocin remained high. The contents of beta-endorphin and enkephalin decreased gradually in non-infectious group, but were still higher than normal. The most obvious change was seen in beta-endorphin, suggesting that beta-endorphin plays a more important role in trauma. This was also confirmed in rat injury model.
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PMID:[Clinical and experimental studies of the dynamic changes in neuropeptides after trauma]. 784 24

The effects of intracerebroventricular injection of Anti-opioid peptide sera on oxytocin-induced enhancement of electroacupuncture (EA) analgesia were observed in this study. It was found that injection of anti-beta-endorphin serum (AEPS) alone could attenuate EA analgesia in rats. Injection of AEPS prior to intraventricular injection of oxytocin could not block the enhancement of EA analgesia by oxytocin. The antidynorphin A1-13 serum (ADYNS) alone could also reduce the EA analgesia, whereas injection of ADYNS prior to injection of oxytocin could potentiate the enhancement of EA analgesia by oxytocin. However, neither the anti-methionine enkephalin serum nor the anti-leucine enkephalin exerted any effect on the enhancement of EA analgesia by oxytocin. The above results showed that the dynorphin attenuate oxytocin-induced enhancement of EA analgesia, but Beta-endorphin and enkephalin do not affect this role of oxytocin. These data suggest the enhancement of EA analgesia by oxytocin is not dependent upon the endogenous pioid peptides in brain.
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PMID:[Effect of anti-opioid peptide sera on oxytocin-induced enhancement of electroacupuncture analgesia]. 790 15

Because of the enormous growth over the last three decades of research on the role of peptides in the brain, the need became apparent to determine the status of these compounds in terms of their current research interest. Since 1965, over a quarter of a million research papers have been published on peptides that have since been classified as neuroactive. The present study was undertaken to analyze systematically the yearly trends of research emphasis in neuroactive peptides as reflected by their individual frequency of publication by year, beginning in 1966. A computer analysis of the publication characteristics was carried out using the Medline data base in which the citation search was limited to the topic brain crossed with the topic mammal. One criterion for the inclusion of a given peptide in the analysis was a frequency of 25 or more citations following its discovery, as related to the mammalian brain. The 42 peptides that met this criterion were: adrenocorticotropic hormone, angiotensin II, atrial natriuretic factor, bombesin, bradykinin, calcitonin, calcitonin gene-related peptide, carnosine, beta-casomorphin, cholecystokinin, corticotropin-releasing factor, delta sleep-inducing peptide, dynorphin, beta-endorphin, Leu-enkephalin, Met-enkephalin, galanin, gastrin, glucagon, growth hormone, growth hormone-releasing factor, insulin, kyotorphin, beta-lipotropin, luteinizing hormone-releasing factor, melanocyte-stimulating hormone release inhibitory factor-1, alpha-melanocyte-stimulating hormone, motilin, neurokinin A, neurokinin B, neuropeptide Y, neurotensin, oxytocin, pituitary adenylate cyclase activating polypeptide, peptide HI, prolactin, secretin, somatostatin, substance P, thyroid-releasing hormone, vasopressin, and vasoactive intestinal peptide. An overall analysis of the 298,105 papers published on these 42 peptides since 1965 revealed that the research activity of 24,742, or 8.30%, of the studies, focused on their neuroactive properties. Taken as a whole, the research on neuroactive peptides reached a peak in 1986, as reflected by the total of 1793 papers published during that year. Although the level of publication has fluctuated between 1548 and 1774 research papers over the last 6 years, it is now clear that the trend in research on neuroactive peptides has reached an asymptote today that shows no sign of deviation. A temporal analysis year by year of individual publication profiles revealed three distinct trends: 1) peptides showed a slow development in research interest and did not exceed more than 15-30 publications per year; 2) peptides exhibited a steady increase in research activity over the years that continues today; and 3) peptides displayed an initial, often intense, research emphasis that inexplicably declined, in some cases precipitously, in the mid 1980s.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuroactive peptides: unique phases in research on mammalian brain over three decades. 800 41

Previous studies have suggested an involvement of enkephalins in regulation of oxytocin (OXT) and vasopressin (AVP) release, which seems to disagree with the very low affinities of Met- and Leu-enkephalin for the kappa opioid receptor. As opioid receptors in the neural lobe exclusively exist of kappa receptors, we studied the binding characteristics of larger pro-enkephalin derived peptides for opioid binding sites in the neural lobe by means of light microscopic receptor autoradiography. In addition, the pharmacological characteristics of opioid binding sites in the neural lobe were compared with those in other parts of the pituitary. In the neural as well as the intermediate lobe both high and low affinity 3H-bremazocine binding sites were present. Binding to these sites was completely displaceable by both naloxone and nor-binaltorphimine suggesting that these sites represent kappa opioid receptors. Also with regard to selectivity and affinity characteristics to other ligands, opioid binding sites in the neural and intermediate lobe were quite similar. In the anterior lobe a very low level of bremazocine binding was present, which could not be displaced by nor-binaltorphimine. Displacement studies with pro-enkephalin and pro-dynorphin derived peptides showed that both groups of peptides could bind to opioid binding sites in the neural and intermediate lobe. Especially the relatively large pro-dynorphin and pro-enkephalin derived peptides, such as dynorphin 1-17 and BAM22, appeared to be very potent ligands for these opioid binding sites and were much more potent than smaller fragments, such as dynorphin 1-8, and Met- and Leu-enkephalin. These results contradict the existence of a mismatch in the neural (and intermediate) lobe with regard to the local type of opioid peptides and receptors present.
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PMID:Characterization of opioid binding sites in the neural and intermediate lobe of the rat pituitary gland by quantitative receptor autoradiography. 802 68


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