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)

Both opioid peptides such as beta-endorphin and met-enkephalin and nonopioid peptides such as vasopressin and oxytocin increase pain thresholds in rodents. Antisera raised against each of these peptides have been developed for use in immunocytochemical and radioimmunoassay procedures. The present study assessed whether central administration of antisera raised against beta-endorphin (ABE), met-enkephalin (AME), arginine, vasopressin (AAVP) or oxytocin (AOT) altered tail-flick latencies elicited by three different levels of radiant heat, jump thresholds, core body temperatures and locomotor activity. ABE induced a transient hyperalgesia on the tail-flick test at thermal levels at which beta-endorphin administration would elicit an analgesic effect. While met-enkephalin increases tail-flick latencies elicited by high thermal levels, AME failed to alter latencies at this level, but rather induced a short-acting hyperalgesia at a low thermal level. While vasopressin increased tail-flick latencies at high thermal levels, AAVP produced reciprocal decreases. Yet AAVP inexplicably induced analgesic effects at moderate and low thermal levels. Finally, while oxytocin increased latencies at high thermal levels, AOT failed to alter latencies. Rather, it decreased latencies at the moderate thermal level and increased latencies at the low thermal level. Neither jump thresholds nor core body temperatures were affected by any antiserum pretreatment. While activity levels were unaffected by either ABE, AME or AAVP pretreatment, AOT decreased activity in a fashion complementry to oxytocin-induced hyperactivity and seizures. There data are discussed in terms of tonic versus phasic influences of these peptides upon pain perception.
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PMID:Pain threshold changes in rats following central injection of beta-endorphin, met-enkephalin, vasopressin or oxytocin antisera. 609 76

Plasma prolactin, growth hormone, cortisol, luteinising-hormone-releasing hormone (LHRH), thyrotropin-releasing hormone (TRH), and nicotine and oestrogen stimulated neurophysin (NSN and ESN) were measured before and for 6 min after electroconvulsive therapy (ECT) in eight women with severe electroconvulsive therapy (ECT) in eight women with severe depression. Plasma concentrations of NSN and ESN had increased significantly (as much as 10-fold for NSN) within 1 min of the seizure, and concentrations of prolactin had increased within 2-4 min after the seizure. Whereas plasma prolactin and ESN either continued to increase or remained raised throughout the 6 min after seizure, the concentrations of NSN fell to reach a value at 6 min that was approximately 50% of the maximum. There were no increases in any of the other hormones or peptides within the 6 min period under study. Thus ECT has selective effects on hormone release which cannot be attributed simply to a generalised release of pituitary or hypothalamic hormones in response to brain stimulation and/or stress.
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PMID:Immediate increases in plasma prolactin and neurophysin but not other hormones after electroconvulsive therapy. 612 44

The cases of 2 women undergoing induced abortions in the 16th week of gestation who developed hyponatremia and grand mal-like seizures during administration of oxytocin are described. The women, aged 22 and 16, received 50 mg synthetic prostaglandin F2alpha (PGF2alpha), Amoglandin, intraamniotically, as well as intravenous infusions of 5% glucose with synthetic oxytocin, Syntocinon, 100 I.U./1000 ml. 25 and 26 hours later the 2 patients had typical grand mal-like seizures followed by postictal sleep. The patients had received total doses of 400 and 200 I.U. of oxytocin. The oxytocin infusions were stopped and .9% NaC1 solution was administered intravenously. Both patients were discharged fully recovered after 4 days. Synthetic oxytocin is known to have a dose-dependent antidiuretic effect during intravenous infusion, even in doses as low as 10 mU/minute. The routine use of oxytocin for midtrimester abortion was discontinued by the authors after the cases occurred.
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PMID:Prostaglandin-oxytocin induction of mid-trimester abortion complicated by grand mal-like seizures. 640 73

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

When vasopressin is administered into the lateral ventricles of rats it produces severe convulsive activity characterized by a rapid barrel rotation. Electrical recordings from the dorsal hippocampus indicate marked elevations in the amplitude and frequency at doses of 5 microliter of 2 x 10(-5) M vasopressin. No significant behavioral effects were noted with oxytocin, somatostatin, beta-melanophore-stimulating hormone, adrenocorticotropin, or leu-enkephalin. Pretreatment of the rats with intraventricularly administered oxytocin, beta-MSH, or systemically administered Dilantin prevented the vasopressin-induced seizures. With the use of chemical and enzymic modification procedures, the essential fragment and amino acids of vasopressin needed for the activity were determined. It was concluded that although the peptide could be acting by vasoconstricting blood arterioles and capillaries in the brain, it may also be exerting a direct excitatory action on neurons.
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PMID:Chemical requirements of vasopressins for barrel rotation convulsions and reversal by oxytocin. 740 Nov 98

The time course and extent of changes in plasma prolactin, noradrenaline, vasopressin and oxytocin levels is reported following serial observations of a prolonged epileptic seizure arising in the temporal lobe, recorded by video-EEG-telemetry, in which the epileptic activity evolved from a simple partial to complex partial to secondarily generalised attack. The prolactin levels were markedly elevated during the phase of the simple partial seizure, at a time when consciousness was preserved, when motor activity was minimal and when EEG activity was highly localised. The hormonal levels continued to rise during the subsequent seizure evolution, suggesting that the duration (or intensity) of the seizure is an important, perhaps the most important, factor determining the degree of prolactin release during limbic seizures. Indeed, the prolactin elevation in this case (26 times the baseline level) is higher than any previously recorded, reflecting the unusual duration and intensity of this seizure. We did not observe the phenomenon of "exhaustion" of prolactin release and levels peaked after 49 min, and were high for over 2 h after the onset of the seizure, and after the convulsion had ceased. The concentrations of vasopressin, oxytocin and noradrenaline remained low during the aura, but rapidly increased during the phase of generalisation. The oxytocin and noradrenaline levels peaked during the phase of generalised convulsion, but the vasopressin levels peaked well into the post ictal phase, and remained high for several hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations of prolactin, noradrenaline, vasopressin and oxytocin during and after a prolonged epileptic seizure. 780 41

The general pharmacological properties of a novel cognition-enhancing agent, nefiracetam (N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide, DM-9384, CAS 77191-36-7) were investigated, and the following results were obtained. 1. Central nervous system: Nefiracetam showed depressant activities (such as ataxia) on general behavior (mice), and inhibited spontaneous locomotor activity, rota-rod and traction performances (mice) and polysynaptic potential of the spinal reflex (rats), and potentiated pentobarbital anesthesia (mice). The drug inhibited electroshock-induced seizure at relatively low doses, but did not affect chemoshock-induced seizure (mice). Nefiracetam failed to show analgesic activity in the tail pinch test, but inhibited the acetic acid-induced writhing syndrome (mice). An inhibitory pattern in the electroencephalogram was observed (cats). Nefiracetam had little or no effect on body temperature (rats). 2. Respiratory and cardiovascular systems: Nefiracetam induced transient decreases in blood pressure, left ventricular pressure and LV dp/dt max at higher doses (dogs). 3. Autonomic nervous system: Nefiracetam had no influence on pupil size (rabbits). The drug induced no significant effect on the pressor response to norepinephrine or depressor response to acetylcholine, but inhibited the contractile response of the nictitating membrane to preganglionic cervical sympathetic nerve stimulation at the highest dose (dogs). 4. Gastrointestinal system: Nefiracetam inhibited gastrointestinal propulsion (mice), gastric emptying rate and gastric secretion (rats) at higher doses. Nefiracetam produced no apparent damage in the gastric mucosa, and had no effect on bile secretion (rats). 5. Isolated smooth muscle: Nefiracetam had no effect on the resting tonus of isolated ileum, whereas it inhibited the contractile response to acetylcholine, histamine, serotonin, nicotine and BaCl2 at higher concentrations (guinea pigs). Nefiracetam had no effect on the resting tonus or the serotonin-induced contraction of stomach fundus (rats). The drug had no effect on the resting tonus or the norepinephrine-induced contraction of vas deferens, but tended to inhibit the contraction induced by nerve stimulation (guinea pigs). Nefiracetam had little or no effect on the resting tonus or oxytocin-induced contraction of virgin uterus, or on spontaneous contraction of pregnant uterus (rats). Nefiracetam did not affect the resting tonus of trachea, whereas it inhibited isoproterenol-induced relaxation at the highest concentration (guinea pigs). Nefiracetam had no chronotropic effect in isolated atria, but showed a slight negative inotropic effect at the highest concentration (guinea pigs). 6. Miscellaneous: Nefiracetam slightly decreased urinary volume, whereas it did not affect urinary electrolyte excretion (rats).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:General pharmacological profile of the new cognition-enhancing agent nefiracetam. 801 90

Due to the complex nature of generalized limbic seizures, marked disturbances in physiological homeostasis occur. Accompanying the motor manifestations which characteristically are associated with generalized limbic seizures, alterations in neuroendocrine, behavioral, and autonomic functions may be observed. The paraventricular nucleus (PVN) of the hypothalamus is known to play a significant role in such neuronal responses to stressful stimuli; however, the effect of seizures on hypothalamic neurons is unknown. We have used the immunocytochemical detection of the Fos protein to anatomically identify neurons in the PVN which are activated following generalized limbic seizures. To induce seizures, rats received intraperitoneal injections of kainic acid or were kindled from the entorhinal cortex. We have demonstrated that elicitation of generalized limbic seizures induces a dramatic number of neurons in the PVN to express the Fos protein. Numerous Fos-immunolabeled neurons were identified in both the parvicellular and magnocellular component of the PVN. In the latter, this study clearly reveals a preferential and selective activation of oxytocin-containing neurons, and it extends and supports the hypothesis that oxytocin plays a role in the body's response to specific stress paradigms. Data suggest that an activation of the oxytocin neuronal system may be part of the adaptive mechanism that enables the hypothalamus to modulate and maintain an adequate response to stressors (e.g., generalized seizures) to regain homeostasis.
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PMID:Activation of oxytocin-containing neurons of the paraventricular nucleus (PVN) following generalized seizures. 885 16

In this study, the regulation of hypothalamic oxytocin and vasopressin messenger RNA expression following the induction of seizures was investigated by in situ hybridization. Following kainic acid-induced seizures, a significant increase in oxytocin messenger RNA in the paraventricular nucleus was demonstrated at 1.5 h, one and two weeks; its level decreased at three weeks and was significantly increased again at four weeks; at eight weeks the messenger RNA level still remained higher than that of controls. Vasopressin messenger RNA in the paraventricular nucleus was increased significantly only at 1.5 h following induction of seizures. The oxytocin messenger RNA level in the supraoptic nucleus was also increased early at 1.5 h and later at four weeks following seizures; however, these increases did not last as long as those in the paraventricular nucleus. Vasopressin messenger RNA in the supraoptic nucleus was also increased after the initial seizures; however, its messenger RNA level vacillated up and down throughout the post-seizure times studied. The earliest significant increase of vasopressin messenger RNA was at one week after seizures, and there was a late significant increase of vasopressin messenger RNA at three weeks after seizures. The present study demonstrates that following kainic acid-induced seizures both, the oxytocin and vasopressin messenger RNA expressions, were up-regulated and these up-regulations were long-term events. The increase of oxytocin messenger RNA in the paraventricular nucleus was more persistent than the others. The pattern of messenger RNA up-regulation was different for oxytocin and vasopressin, and different in the paraventricular nucleus and supraoptic nucleus. These different patterns of messenger RNA elevations suggest that the different components of the rat hypothalamus were regulated differentially by kainic acid-induced seizures.
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PMID:Oxytocin and vasopressin mRNA expression in rat hypothalamus following kainic acid-induced seizures. 905 6

Intractable temporal lobe epilepsy is a disabling disorder with far reaching effects on brain function, behavior and neuroendocrine function. Previous work in the kindled-seizure model for temporal lobe epilepsy has shown that these seizures cause vasopressin (VP) release, an increase in resting VP and lasting increases in VP mRNA in the supraoptic nucleus (SON) of the hypothalamus. In this study we used in situ hybridization to examine the effects of kindled seizures on the expression of two other functionally-related, neuroendocrine genes, oxytocin (OT) and corticotrophin releasing factor (CRF). Comparisons in kindled and sham-stimulated controls revealed an increase in VP mRNA but not OT mRNA in magnocellular neurons and an increase in CRF mRNA in parvocellular neurons of the paraventricular nucleus (PVN) of the hypothalamus 1 month after the last seizure. We conclude that kindled seizures induce selective changes in neuroendocrine gene expression in neuroendocrine systems, VP and CRF but not OT.
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PMID:Persistent elevation of corticotrophin releasing factor and vasopressin but not oxytocin mRNA in the rat after kindled seizures. 913 93


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