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 neurotransmitter gamma-aminobutyric acid (GABA) appears to be involved in the control of gonadotropin secretion. These studies were conducted 1) to evaluate the effect of GABAergic drugs on in vitro LHRH secretion and 2) to characterize the role of different types of GABA receptors (the GABA-A and GABA-B subtypes) in these actions. Arcuate nuclei-median eminence fragments were incubated in vitro, and the release of LHRH, prostaglandin E2 (PGE2), arginine vasopressin, and oxytocin was measured by RIA. Both GABA and muscimol at different concentrations induced an increase in LHRH release, but did not affect the release of arginine vasopressin and oxytocin. This stimulatory effect was blocked by the specific GABA antagonist bicuculline, suggesting the involvement of GABA-A type receptors. Muscimol-stimulated LHRH release was not affected by the presence of phentolamine, suggesting that the stimulatory effect of GABA-A receptors on LHRH release is not mediated by interactions with the noradrenergic system. PGE2 has been shown to be a potent secretagogue of LHRH from the median eminence in vitro, and in this model the stimulatory effect of PGE2 was enhanced by muscimol. Baclofen, a specific GABA-B type receptor agonist, had no effect on basal LHRH release, but completely suppressed naloxone-stimulated LHRH and PGE2 secretion. The inhibitory effect of baclofen was blocked by the presence of 5-aminovalerate, a drug that has been shown to block the inhibitory effect of baclofen on NE release from noradrenergic terminals. This suggests the possibility that GABA-B receptors interacting with noradrenergic terminals may be responsible for the inhibitory effect of baclofen on naloxone stimulation. This study uncovered both stimulatory and inhibitory effects of GABA on LHRH release after activation of GABA-A or GABA-B receptors, respectively. Further, the data show possible relationships among the GABAergic, endogenous opiate peptide, and noradrenergic systems in the control of LHRH release from the hypothalamus.
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PMID:Different gamma-aminobutyric acid receptor subtypes are involved in the regulation of opiate-dependent and independent luteinizing hormone-releasing hormone secretion. 254 12

The effect of muscimol and baclofen injected into the paraventricular nucleus of the hypothalamus on penile erection and yawning induced by apomorphine, oxytocin and N-methyl-D-aspartic acid (NMDA) was studied in male rats. Muscimol (20-200 ng), but not baclofen (200 ng), injected into the paraventricular nucleus of the hypothalamus 10 min before apomorphine (50 ng), oxytocin (10 ng) or NMDA (50 ng) reduced penile erection and yawning induced by the above compounds given into the paraventricular nucleus. Bicuculline (250 ng) injected into the paraventricular nucleus 5 min before muscimol (100 ng) prevented the inhibitory effect of muscimol on penile erection and yawning induced by apomorphine, oxytocin and NMDA. The present results show that gamma-aminobutyric acid (GABA) inhibits penile erection and yawning by acting on GABA(A) receptors in the paraventricular nucleus of the hypothalamus.
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PMID:Activation of gamma-aminobutyric acid(A) receptors in the paraventricular nucleus of the hypothalamus reduces apomorphine-, N-methyl-D-aspartic acid- and oxytocin-induced penile erection and yawning in male rats. 1070 59

Male rats show 4-6 penile erection episodes when put in the presence of an inaccessible receptive female. These non-contact penile erections were reduced dose-dependently by muscimol, a gamma aminobutyric acid (GABA)(A) receptor agonist, when given into the paraventricular nucleus of the hypothalamus (0.1, 0.5, 1 and 2 microg). In contrast, baclofen, a GABA(B) receptor agonist (2 microg) was ineffective. Muscimol reduction of non-contact penile erections was not seen when male rats were pretreated with bicuculline methiodide (2 microg) given 5 min before muscimol into the paraventricular nucleus. Since muscimol injected into the paraventricular nucleus also prevents penile erection induced by drugs (e.g. apomorphine, oxytocin or N-methyl-D-aspartic acid), the present results show that an increased GABAergic activity in the paraventricular nucleus can impair the expression of penile erection induced not only by drugs but also by sexual physiological stimuli.
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PMID:The activation of gamma aminobutyric acid(A) receptors in the paraventricular nucleus of the hypothalamus reduces non-contact penile erections in male rats. 1170 99

The effect of muscimol, a GABAA receptor agonist, injected into the paraventricular nucleus (PVN) of the hypothalamus on drug-induced (apomorphine, oxytocin and NMDA) yawning and penile erection, and on the increase in the concentration of NO2- and NO3- occurring in the paraventricular dialysate in these experimental conditions, was studied in male rats. Muscimol (50, 100 and 200 ng) reduced, in a dose-dependent manner, penile erection and yawning induced by apomorphine (50 ng), oxytocin (30 ng) and NMDA (50 ng) delivered into the PVN. The reduction of penile erection and yawning was parallel to a reduction of the concomitant NO2- and NO3- increase that occurs in the paraventricular dialysate in this experimental condition. In contrast, baclofen (200 ng), a GABAB receptor agonist, was ineffective. The muscimol effects on drug-induced penile erection, yawning and NO2- increase were prevented by the prior administration of bicuculline (250 ng into the paraventricular nucleus). Muscimol (200 ng) but not baclofen (200 ng), injected into the PVN, reduced both noncontact erections in male rats placed in the presence of an inaccessible receptive female, and also the NO2- increase that occurs in the paraventricular dialysate in this experimental condition. As found with drug-induced penile erection, the muscimol reduction of noncontact erections and of NO2- increase was prevented by bicuculline. The present results show that the activation of GABAA receptors in the PVN reduces yawning and penile erection induced by drugs or physiological stimuli by reducing the increase in NO activity that occurs in this hypothalamic nucleus in these experimental conditions.
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PMID:Reduction of drug-induced yawning and penile erection and of noncontact erections in male rats by the activation of GABAA receptors in the paraventricular nucleus: involvement of nitric oxide. 1190 27

We investigated the involvement of GABAergic mechanisms of the central amygdaloid nucleus (CeA) in unanesthetized rats subjected to acute isotonic or hypertonic blood volume expansion (BVE). Male Wistar rats bearing cannulas unilaterally implanted in the CeA were treated with vehicle, muscimol (0.2 nmol/0.2 microL) or bicuculline (1.6 nmol/0.2 microL) in the CeA, followed by isotonic or hypertonic BVE (0.15 or 0.3 M NaCl, 2 mL/100 g body weight over 1 min). The vehicle-treated group showed an increase in sodium excretion, urinary volume, plasma oxytocin (OT), and atrial natriuretic peptide (ANP) levels compared to control rats. Muscimol reduced the effects of BVE on sodium excretion (isotonic: 2.4 +/- 0.3 vs vehicle: 4.8 +/- 0.2 and hypertonic: 4.0 +/- 0.7 vs vehicle: 8.7 +/- 0.6 microEq.100 g-1.40 min-1); urinary volume after hypertonic BVE (83.8 +/- 10 vs vehicle: 255.6 +/- 16.5 microL.100 g-1.40 min-1); plasma OT levels (isotonic: 15.3 +/- 0.6 vs vehicle: 19.3 +/- 1 and hypertonic: 26.5 +/- 2.6 vs vehicle: 48 +/- 3 pg/mL), and ANP levels (isotonic: 97 +/- 12.8 vs vehicle: 258.3 +/- 28.1 and hypertonic: 160 +/- 14.6 vs vehicle: 318 +/- 16.3 pg/mL). Bicuculline reduced the effects of isotonic or hypertonic BVE on urinary volume and ANP levels compared to vehicle-treated rats. However, bicuculline enhanced the effects of hypertonic BVE on plasma OT levels. These data suggest that CeA GABAergic mechanisms are involved in the control of ANP and OT secretion, as well as in sodium and water excretion in response to isotonic or hypertonic blood volume expansion.
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PMID:GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats. 1921 4