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)

Intrathecal (IT) injection of arginine vasopressin (AVP) in rats caused a transient (less than 30 min), dose-related paralysis of the hindlimbs, loss of hindlimb and tail nociceptive responsiveness, and increased mean arterial pressure. Motor dysfunction was produced with comparable potency by lysine vasopressin (LVP) and arginine vasotocin (AVT); oxytocin (OXY) was approximately 1000 times less potent. Paralysis induced by these peptides was selectively blocked following IT pretreatment with 0.5 nmoles of the vasopressin V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine] Arg8-vasopressin (d(CH2)5[Tyr(Me2)]AVP). Pressor and antinociceptive responses to AVP were also blocked by this compound. However, at higher doses (2-5 nmoles, IT), d(CH2)5[Tyr(Me2)]AVP produced hindlimb paralysis, antinociception, and pressor responses by itself. In contrast to the fiber degeneration, cell loss, and necrosis found in lumbosacral cords of rats persistently paralyzed by other peptides (dynorphin A, somatostatin, and ICI 174864), neuropathological changes were not evident in spinal cords of rats transiently paralyzed by IT AVP. These results indicate that AVP-related peptides affected diverse spinal cord functions through interactions with a V1-like receptor. The similar pattern of cardiovascular and antinociceptive responses to other peptides (dynorphin A, somatostatin, and ICI 174864), which also caused hindlimb paralysis, suggests that the former responses may actually reflect the nonselective consequences of a peptide-induced disruption of spinal cord function, rather than specific shared pharmacological effects.
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PMID:Hindlimb paralytic effects of arginine vasopressin and related peptides following spinal subarachnoid injection in the rat. 324 52

1. Rats underwent either: (1) acute or chronic morphine or naloxone administration; (2) simple morphine withdrawal or naloxone-precipitated withdrawal in morphine-dependent animals; or (3) stress from I.P. administration of hypertonic saline. 2. Quantitative in situ hybridization histochemistry was performed using synthetic oligonucleotide probes for corticotrophin-releasing factor (CRF), vasopressin, pro-opiomelanocortin (POMC), dynorphin, enkephalin and oxytocin mRNAs. The paraventricular and supraoptic nuclei were examined in all studies and the arcuate nucleus and pituitary gland in the acute withdrawal study. 3. Neither acute nor chronic morphine administration altered either (a) hypothalamic parvocellular or magnocellular CRF mRNA, or (b) anterior pituitary or pars intermedia POMC mRNA. 4. Naloxone-precipitated morphine withdrawal resulted in a marked increase in parvocellular (but not magnocellular) CRF mRNA within 4 h and levels remained elevated through 24 h. There was no change in arcuate nucleus or pars intermedia POMC mRNA, but in the anterior pituitary there was a delayed increase, significant at 24 h. 5. Simple morphine withdrawal without the use of naloxone did not result in any change in CRF mRNA but there were increases in magnocellular vasopressin and dynorphin mRNA, presumably related to decreased water intake. 6. Intraperitoneal hypertonic saline stress also resulted in a marked accumulation of both parvocellular CRF and vasopressin mRNA without any concomitant change in magnocellular vasopressin mRNA. Increased translation of CRF mRNA was also evidenced by increased immunoreactive CRF detected by immunocytochemistry.
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PMID:Corticotrophin-releasing factor, vasopressin and pro-opiomelanocortin mRNA responses to stress and opiates in the rat. 326 21

We examined opioid binding in fractions with disconnected nerve endings (secretosomes) which were prepared from porcine neurohypophyses by centrifugation in a discontinuous Percoll gradient. Specific (= displaceable) binding was observed with 3H-etorphine and with 3H-diprenorphine, two ligands with low selectivity for distinct opiate receptor subclasses. No displaceable binding was found with the prototypic mu- and delta-ligands 3H-dihydromorphine and 3H-(D-Ala, D-Leu) enkephalin. Displacement of 3H-diprenorphine binding was almost absent with the selective mu- and delta-ligands morphiceptin and ICI-174864. Partial displacement occurred with the selective kappa-ligand U-50488 and with dynorphin. Binding of 3H-etorphine was stereo-specific. 3H-diprenorphine binding was saturable with a KD between 2 and 4 nM. Maximum of opiate binding activity was detected in the fractions with accumulated secretosomes. By autoradiography specific 3H-diprenorphine binding is shown to be mainly associated with secretosomes. In imunocytochemical preparations an oxytocin antibody was immunoreactive in 85% of the secretosomes in the fraction with highest opiate binding. These fractions in radioimmunoassays exhibited the largest contents in oxytocin and low vasopressin levels. The data therefore suggest that in the porcine neurohypophysis opioid binding sites of the kappa-type occur in secretory endings presumably of the oxytocin type.
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PMID:Opiate binding differentially associated with oxytocin and vasopressin nerve endings from porcine neurohypophyses. 340 60

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

We investigated the effects of dopamine, met-enkephalin and leu-enkephalin on basal and ouabain-stimulated release of oxytocin and vasopressin from isolated neurointermediate lobes. The present study revealed that neurohypophyseal hormone release was not affected by dopamine, neither from lobes of untreated rats nor from those of rats with dopamine-deficiency (pretreated with alpha-methyl-p-tyrosine-methylester). Likewise, metoclopramide, a dopamine antagonist, was unable to alter the neurohypophyseal hormone release. Our results also indicate that the opioid peptides met-enkephalin and leu-enkephalin do not influence spontaneous or ouabain-stimulated oxytocin and vasopressin release, which is in accordance with our findings that naloxone under our experimental conditions is also ineffective.
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PMID:Lack of response in the release of oxytocin and vasopressin from isolated neurohypophyses to dopamine, met-enkephalin and leu-enkephalin. 609 Jan 93

The opioid peptide dynorphin is widely distributed in neuronal tissue of rats. By immunocytochemical methods, it was shown previously that dynorphin-like immunoreactivity is present in the posterior pituitary and the cells of the hypothalamic neurosecretory magnocellular nuclei which also are responsible for the synthesis of oxytocin, vasopressin, and their neurophysins. By using an affinity-purified antiserum to the non-enkephalin part of the dynorphin molecule it has now been demonstrated that dynorphin and vasopressin occur in the same hypothalamic cells of rats, whereas dynorphin and oxytocin occur in separate cells. Homozygous Brattleboro rats (deficient in vasopressin) have magnocellular neurons that contain dynorphin separate from oxytocin. Thus dynorphin and vasopressin, although they occur in the same cells, appear to be under separate genetic control and presumably arise from different precursors.
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PMID:Dynorphin and vasopressin: common localization in magnocellular neurons. 612 76

The pars intermedia of the pituitary in the rabbit and hare is abundantly innervated by axons reacting selectively with antibodies against oxytocin. These axons contain dense secretory vesicles about 140 nm in diameter, i.e., smaller than those in the neurosecretory axons of the neural lobe. No fiber elements staining for other peptides (vasopressin, somatostatin, substance P) were observed in the pars intermedia, except rare leu-enkephalin axons restricted to the rostral zone of the gland. Dopaminergic innervation appears to be completely absent from the intermediate lobe. This was shown by the lack of reaction with an antibody against tyrosine-hydroxylase, which did reveal a well-developed tubero-infundibular system of nerve fibers. Axons reacting with an antibody against serotonin were irregularly distributed in the pars intermedia. In the absence of dopaminergic axons, the extensive oxytocin-like innervation may play a major role in regulating the melanotrophic cell activity in the Leporidae.
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PMID:Oxytocin-immunoreactive nerve fibers in the pars intermedia of the pituitary in the rabbit and hare. 613 Aug 46

The very potent opioid peptide, dynorphin, has recently been shown by radioimmunoassay and immunocytochemical techniques to be selectively concentrated in the pars nervosa of pituitary, suggesting a possible association of dynorphin with the neurohypophyseal hormones, vasopressin and oxytocin. In this study, we report that pituitary and brain contents of immunoreactive dynorphin in homozygote Brattleboro rats (unable to synthesize vasopressin) are similar to those in heterozygote animals and in normal Long-Evans rats. Thus, the syntheses of immunoreactive dynorphin and vasopressin in the hypothalamo-hypophyseal tract appear to be independently regulated.
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PMID:Levels of immunoreactive dynorphin in brain and pituitary of Brattleboro rats. 613 55

beta-Endorphin (200ng), dynorphin1-17 (2 micrograms) and morphine (4 micrograms) suppressed the osmotically-evoked release of oxytocin in anaesthetized lactating rats. ACTH1-24 (0.2-3 micrograms) administered intraventricularly 3 min before beta-endorphin or morphine attenuated their inhibitory action, but when applied afterwards was never seen to reverse their effects although this was achieved with naloxone (lmg X kg-1, i.v.). ACTH however, was ineffective against dynorphin. At higher doses an opiate-like action of ACTH was observed. Thus ACTH may act as a partial antagonist and at higher doses as a partial agonist of the opiate receptor for which it is known to have an affinity. It is suggested that suppression of oxytocin release by endogenous beta-endorphin could be modified by ACTH with which it may be co-released.
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PMID:Effect of ACTH on opiate inhibition of oxytocin release. 614 96

The present study examines the relationship of the hypothalamic paraventricular nucleus (PVN) to discrete brain and pituitary pools of immunoreactive (ir) vasopressin (VP), oxytocin (OT) and particular opioid peptides in the rat. Selective, bilateral destruction of the PVN resulted in a parallel depression in levels of ir-VP, ir-OT, ir-dynorphin (DYN), ir-DYN and ir-alpha-neo-endorphin (alpha-NE) in the neurointermediate lobe of the pituitary, whereas in its anterior counter-part no decrease in the content of any of these peptides was seen. In contrast, the content of ir-beta-endorphin (beta-EP) in the neurointermediate lobe was not significantly altered. Further, a rise in levels of ir-beta-EP in the anterior lobe, together with a fall in these in systemic plasma, was found. In the hypothalamus, in distinction to ir-met-enkephalin (ME), a diminution in the content of ir-VP, ir-OT, ir-DYN, ir-DYN, ir-alpha-NE and, in addition, ir-beta-EP was observed. In the septum, midbrain and medulla/pons, however, a selective depression in levels of ir-VP (and, as measured in the medulla/pons, of ir-OT) was seen: the content of ir-DYN, ir-DYN, ir-alpha-NE, ir-beta-EP and ir-ME was unchanged in these tissues. These data indicate that: (1) the PVN is an important contributor to neurointermediate lobe, but not anterior lobe, pools of ir-VP, ir-OT, ir-DYN, ir-DYN and ir-alpha-NE in contrast to ir-beta-EP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hypothalamic paraventricular nucleus: relationship to brain and pituitary pools of vasopressin and oxytocin as compared to dynorphin, beta-endorphin and related opioid peptides in the rat. 614 57


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