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)

The mechanisms of lymphatic-vascular transfer across the ovarian vascular pedicle were studied in anaesthetized sheep 8-15 days after ovulation. [3H]Prostaglandin F2 alpha (PGF2 alpha), [14C]mannitol and [36Cl]Na were infused continuously into either a uterine lymphatic or a uterine vein and the kinetics of transfer into the adjacent utero-ovarian vein or ovarian plasma were studied. Transfer occurred according to the sequence [36Cl] greater than [14C] greater than [3H] indicating that PGF2 alpha is not transferred by rapid diffusion, as with [36Cl]Na, nor by a paracellular route, as with [14C]mannitol, but by a slower process probably involving facilitated diffusion. Transfer into the adjacent utero-ovarian vein or ovarian blood was greater when compounds were infused into a uterine lymphatic than into a uterine vein. Substantially more [3H]PGF2 alpha occurred in the adjacent corpus luteum than either of the other compounds after a lymphatic infusion. Intra-lymphatic infusion of PGF2 alpha stimulated the release of ovarian oxytocin but the effect was not confined to the adjacent ovary. Intravenous (jugular) infusion of PGF2 alpha failed to stimulate ovarian oxytocin secretion whereas close-arterial infusion into the ovaries was effective, and the possibility was investigated that any systemic effect of PGF2 alpha was mediated through neural mechanisms. Noradrenaline and acetylcholine were both effective in causing the release of ovarian oxytocin when infused close-arterially into the ovary. With infusions of acetylcholine, ovarian oxytocin secretion rate was increased over fivefold without any change in posterior pituitary release. Noradrenaline and acetylcholine produced a concomitant fall in ovarian blood flow, and neurotransmitter-induced ischaemia may have played a role in ovarian oxytocin release. The finding that PGF2 alpha infused into a uterine lymphatic stimulates ovarian secretion of oxytocin, and that the effect is bilateral whereas PGF2 alpha accumulation in ovarian tissue is unilateral, implies that its mechanism of action may not be solely directed at the luteal cell.
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PMID:Neurotransmitters and lymphatic-vascular transfer of prostaglandin F2 alpha stimulate ovarian oxytocin output in sheep. 276 49

The influences of opioids on oxytocin secretion and parturition were investigated in the rat. Morphine, administered centrally or peripherally, severely delays the course of established parturition. This delay is accompanied by reduced plasma oxytocin levels and is overcome by treatment either with the opioid antagonist naloxone, or by infusion of oxytocin. An endogenous opioid regulatory mechanism inhibiting oxytocin secretion becomes activated immediately prior to and during parturition. This mechanism does not operate earlier in pregnancy or during normal lactation and is not seen in nonpregnant animals. Naloxone acutely speeds up the course of established parturition, an effect accompanied by greatly elevated plasma oxytocin levels. The mechanisms underlying opioid regulation of oxytocin neurones were investigated at two sites. Precipitated withdrawal from chronic morphine treatment causes hypersecretion of oxytocin. This response is mediated by greatly enhanced electrical activity in the perikarya of oxytocin neurones indicating the presence of opioid receptors on oxytocin neurones and/or on their afferent input. Opioid receptors are also present in the neurohypophysis where they exert direct and noradrenaline mediated effects on secretion from oxytocin terminals in vitro.
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PMID:Hypothalamic opioid mechanisms controlling oxytocin neurones during parturition. 284 5

The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline-using the [3H]-noradrenaline technique-from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [3H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7 x 10(-7) M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [3H]-noradrenaline release was maximally enhanced by 41% (ED50 2 x 10(-7) M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The kappa-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [3H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The mu-agonist (D-Ala2, MePhe5 Gly-ol)-enkephalin also failed to inhibit [3H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The delta-agonist (D-Pen2, D-Pen5)-enkephalin was without effect. We conclude that (1) kappa-receptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) kappa-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenergic innervation.
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PMID:Opioid-noradrenergic interactions in the neurohypophysis. I. Differential opioid receptor regulation of oxytocin, vasopressin, and noradrenaline release. 284 91

The function of noradrenaline in the rat neurohypophysis was investigated by examining the effects of selective adrenergic receptor agents on electrically evoked release of oxytocin, arginine vasopressin, and noradrenaline using the [3H]-noradrenaline technique. Since endogenous opioids in the neurohypophysis suppress release of both neurohormones and of noradrenaline, we assessed the role of noradrenaline in mediating opioid actions on neurohormone secretion by examining modification of the action of the opioid antagonist naloxone by adrenergic receptor agents. The data suggest (1) that in addition to opioid receptors, 'presynaptic' alpha 2-receptors regulate release from neurohypophysial noradrenaline terminals; (2) noradrenaline released from neurohypophysial terminals acts on beta- and alpha 1-receptors to facilitate both oxytocin and arginine vasopressin release: this action only becoming evident at elevated levels of endogenous noradrenaline release attained following removal of presynaptic opioid or alpha 2-regulation, and (3) opioid peptides within the neurohypophysis act to inhibit oxytocin and, to a lesser extent, arginine vasopressin secretion, partly through inhibiting release of facilitatory noradrenaline. We propose a model in which opioids act in the neurohypophysis both independently of noradrenaline via kappa-receptors on neurosecretory terminals or pituicytes and also via interaction with the noradrenaline system.
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PMID:Opioid-noradrenergic interactions in the neurohypophysis. II. Does noradrenaline mediate the actions of endogenous opioids on oxytocin and vasopressin release? 284 92

Secretion of the peptide neurohormones oxytocin and vasopressin from terminals of magnocellular neurones in the mammalian neurohypophysis is elicited by conduction of depolarizing action potentials into terminal membranes, inducing opening of voltage-sensitive Ca2+ channels, entry of Ca2+ from the extracellular space and a rise in cytoplasmic Ca2+ concentration. The amount of peptide released per action potential is not immutable. In particular, the patterns in which action potentials are generated at the cell somata of the two types of neurone each appear exquisitely suited to optimize the release process at the terminal by utilizing a frequency-facilitation mechanism and by minimizing a mechanism of fatigue in the release process. The different properties of oxytocin and vasopressin neurones are of important physiological significance. The secretory terminals are also a site of receptor-mediated influences of neuromodulators which can greatly alter release efficiency. The mechanisms underlying facilitation and fatigue are not clearly understood. The evidence suggests that processes both prior to depolarization of the terminals (propagation and form of the action potentials) and directly at the terminals (frequency/pattern-dependent Ca2+ entry and channel openings) are involved. Transient activity-related increases in extracellular K+ concentration may be involved at both sites. Two types of neuromodulation have been partly characterized. Kappa-Opioid receptors in secretory terminal membranes directly modulate depolarization-evoked peptide release probably via interactions with Ca2+ channels. beta-Adrenergic receptors localized on neurohypophyseal astroglial cells mediate more subtle effects of noradrenaline. In the more chronic situation the neurohypophyseal astroglia alter their morphological relationships with neurosecretory elements and the basal lamina at release sites, changes which may also serve to optimize the secretory process.
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PMID:Optimizing release from peptide hormone secretory nerve terminals. 285 Mar 39

A new strategy was devised for the targeted immobilization of ligands on aminohexyl- and carboxyhexyl-agarose. Selectively protected neurotransmitter amino acids and neuropeptides were coupled to amino or carboxyl group-containing agarose derivatives using activated esters, mixed anhydrides or carbodiimides. After coupling, agarose beads were dehydrated and the protecting groups were cleaved in non-aqueous media with acids (trifluoroacetic acid, formic acid). Agarose beads were rehydrated and applied for affinity chromatography and cell surface recognition. The same compounds were coupled to derivatized polyacrylamide beads containing primary amino (Acrylex A), acyl hydrazide (Acrylex AH-100) or carboxyl (Acrylex C-100) groups. Protecting groups were removed by acidolytic cleavage. Oxytocin, vasopressin, tetra- and pentagastrin, cholecystokinin, leucine-enkephalin and carboxyl-bearing derivatives of the neurotransmitters noradrenaline, dopamine, histamine, serotonin, acetylcholine and gamma-aminobutyric acid were immunobilized on agarose and on derivatized polyacrylamide gels.
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PMID:Targeted immobilization of neurotransmitters and neuropeptides on agarose and on Acrylex polymers. 287 23

Oxytocin, vasopressin, melanostatin, bradykinin, LHRH-like peptide in different ways affected the spontaneous outflow and release of adrenaline and noradrenaline induced with central and peripheral nervous stimuli as well as with acetylcholine in the superfusate of the dog isolated inferior mesenteric ganglion.
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PMID:[Peptide modulation of spontaneous and evoked catecholamine release in the caudal mesenteric ganglion of the dog]. 287 2

Synaptic organization of the intermediolateral nucleus of the guinea pig thoracic spinal cord was examined with particular focus on monoamine- and peptide-containing nerve terminals. Axon varicosities having flat synaptic vesicles constituted 17% of all axons in the nucleus and formed exclusively symmetric synapses. Enkephalin-, substance P-, somatostatin-, 5-hydroxytryptamine-, and catecholamine-immunoreactive nerve terminals were densely distributed, while neurotensin, vasoactive intestinal polypeptide-, oxytocin-, and cholecystokinin-8-immunoreactive nerves were sparse in the nucleus. Coexistence of 5-hydroxytryptamine and enkephalin was demonstrated, and coexistence of somatostatin and enkephalin as well as somatostatin and 5-hydroxytryptamine in the same axons was also shown by serial semithin sections. Catecholamine axons labelled by 5-hydroxydopamine formed axodendritic and axosomatic synapses and made direct synaptic contacts on the preganglionic sympathetic neurons identified by retrograde transport of horseradish peroxidase. Direct synaptic contacts from enkephalin- and substance P-immunoreactive axons to preganglionic sympathetic neurons were also revealed. Enkephalin-, substance P-, and 5-hydroxytryptamine-immunoreactive axons formed axodendritic and axosomatic synapses. Catecholamine axon varicosities constituted 19% of all axon varicosities in the nucleus and 30% of them showed synaptic specializations in a sectional plane. Axon varicosities immunoreactive to enkephalin, 5-hydroxytryptamine, and substance P constituted approximately 35, 19, and 13% of all axon varicosities, respectively, while those with synaptic contacts made up 27, 30, and 26%, respectively, in a sectional plane. Enkephalin-, 5-hydroxytryptamine-, and noradrenaline-immunoreactive axons showed mainly symmetric synaptic contacts.
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PMID:Synaptic structure of the monoamine and peptide nerve terminals in the intermediolateral nucleus of the guinea pig thoracic spinal cord. 288 97

The neuroendocrine and neurochemical events which occur in the brain in the context of maternal behaviour fall into two main categories: 1) Those which simultaneously address wide areas of the brain and lack any specific "coding" for maternal behaviour but are nevertheless essential for it to occur. The steroid hormones and rostrally projecting catecholamine systems fall into this category. The steroid hormones may be viewed as primers, but not just for maternal behaviour, while the amines, specifically noradrenaline, act to synchronise a variety of neural systems associated with maternal behaviour. These include the activation of neuroendocrine mechanisms important for the peripheral changes associated with maternal behaviour, an interaction with the oxytocin and beta-endorphin peptidergic systems which are the specific addressing systems, and enhancement of sensory signals and learning contingent upon parturition. Indeed, parturition is the physiological event which activates the noradrenergic system in the context of maternal behaviour. 2) Those which address restricted areas of the brain and may be viewed as specific to maternal behaviour. Their action is dependent on estrogen priming and the noradrenergic synchronisation of other neural events in order for complete maternal behaviour to ensue. The oxytocinergic and beta-endorphin peptidergic systems fall into this category, promoting maternal behaviour and the neural reinforcement associated with this. In order to ensure specificity, these peptidergic systems may be inhibitory to potentially competing behaviours such as sexual behaviour and the reproductive neuroendocrine response associated with it. Although not discussed in this review, the nigrostriatal dopamine projection may be considered both specific, in that it relates only to motor events, and non-specific, in that this relationship exists in all behavioural contexts. Finally, as maternal behaviour progresses, other parts of the brain are called upon to coordinate the different behaviours that become associated with maternalism and ensure protection and feeding of the offspring. The suckling stimulus appears to be important for activating these neural systems by way of the peripeduncular nucleus.
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PMID:Central mechanisms underlying the neural and neuroendocrine determinants of maternal behaviour. 289 99

Opioids intrinsic to the rat neurohypophysial system act to inhibit secretion from the terminals of magnocellular neurones. Opioid receptors in the neurohypophysis are predominantly of the kappa-subtype and selective kappa-agonists suppress electrically evoked release of oxytocin (OXT) and vasopressin (AVP). We have looked for the presence of functional kappa-receptors on neurohypophysial nerve terminals by examining effects of kappa-agonists on secretion from suspensions of isolated neurohypophysial nerve terminals (neurosecretosomes) retained on filters in a perifusion system. Release of both OXT and AVP evoked by K+-depolarisation was inhibited by the kappa-agonists U-50,488H (34% and 45% respectively) and dynorphin A1-13 (68% and 51% respectively). Inhibition by dynorphin A was only observed in the presence of peptidase inhibitors. The actions of both kappa-agonists were prevented by the opioid receptor antagonist naloxone. The experiments indicate the presence of kappa-receptors on terminals of OXT and AVP neurones. This receptor population is in addition to those previously described on pituicytes and those influencing release of neurohypophysial noradrenaline.
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PMID:Functional kappa-opioid receptors on oxytocin and vasopressin nerve terminals isolated from the rat neurohypophysis. 290 8


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