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EN
Healthy, and insulin-deficient (streptozotocin-induced diabetic, STZ) Sprague-Dawley rats were used to investigate the effects of different doses of ß-endorphin (25 and 50 µg/kg) on plasma ß-endorphin, insulin, glucagon, and glucose levels at 15- and 30-min time points. In experimental groups, plasma ß-endorphin levels were higher at the 15-min than at the 30-min time point in healthy rats; however, in STZ-diabetic rats, ß-endorphin levels were lower at 15 min than at 30 min, indicating that intraperitoneal absorption of ß-endorphin differed between healthy and insulin-deficient rats, ß-endorphin did not affect plasma glucose, insulin, or glucagon at either dose in the healthy group. In the insulin-deficient rats, ß-endorphin at 50 µg/kg reduced plasma glucose levels at the 30-min time point compared to the 25 µg/kg dose, without affecting plasma insulin. Moreover, ß-endorphin at 50 µg/kg decreased plasma glucagon levels at the 15-min time point in comparison to the 25 µg/kg dose in insulin-deficient rats. Plasma glucose levels may be reduced in insulin-deficient rats at high ß-endorphin levels regardless of insulin status.
EN
To examine the role of GABAA receptor mediating systems in the control of gonadotropin-releasing hormone (GnRH) release from the ventromedial- infundibular region (VEN/NI) in ewes during luteal phase, the extracellular concentrations of GnRH, ß-endorphin, noradrenaline (NE), dopamine (DA), and their metabolites: MHPG and DOPAC were quantified by local stimulation or blockade of GABAA receptors with muscimol or bicuculline, respectively. Stimulation of GABAA receptors in the VEN/NI did not affect GnRH, ß-endorphin release or catecholaminergic system activity. Blockade of GABAA receptors decreased ß-endorphinergic and dopaminergic activity, and lowered the extracellular concentration of MHPG. It did not affect GnRH release or luteinizing hormone (LH) secretion. It is suggested that progesterone-induced GABAergic activity during the luteal phase may desensitize GABAA receptors to muscimol. Lack of changes in GnRH/LH secretion with concomitant depressed ß-endorphinergic activity corroborated the conclusion that ß-endorphin does not inhibit GnRH release from the VEN/NI during the luteal phase. The physiological significance of changes in the catecholaminergic system activity under GABAA receptor blockade in the control of GnRH secretion awaits to be established.
EN
Opioid peptides are the most effective drugs in controlling pain; their action is elicited by binding to specific membrane receptors. The gastrointestinal tract represents, after the nervous system, the site in which the opioid receptors are expressed at high levels. The opioid agonist morphine has a significant inhibitory effect on intestinal motility, this action is blocked by naloxone an opioid antagonist mainly active at mu and kappa receptors. In this study the presence of mu opioid receptor on rabbit jejunum was investigated by western blot. The effects of beta-endorphin, the endogenous opioid peptide with the highest affinity to the mu opioid receptor and those of naloxone on spontaneous rabbit jejunum contractions were evaluated. Beta-endorphin (10-6M) showed a relaxant effect on jejunum contractility while naloxone showed a dual effect inducing an increase of spontaneous contractility at low concentrations (10-6M, 10-7M, 10-8M) and a decrease when high concentrations (10-3M, 10-4M, 10-5M) were utilized. The obtained results demonstrate that mu opioid receptor is expressed in rabbit jejunum and suggest that this receptor may be involved in mediating the effects of both opioid agonist and antagonist on jejunum contractions.
EN
The possible physiological role of testicular opioid peptides in the control of testicular functions has been studied. In neonatal rats in tratest icular administration of opiate receptor antagonists (naloxone, nalmefene) stimulates Sertoli cell proliferation and secretion. Both in adult and neonatal rats local injection of the testis with opiate receptor antagonists or with ß-endorphin antiserum results in a decrease in steroidogenesis in long-term studies. Treatment of neonatal testis with an enkephalin analogue induces a short-term suppression of testosterone secretion. Further studies were carried out to investigate whether the above described local effects of opiate agonist or antagonist on testicular function are under the regulatory control of testicular nerves. Partial denervation of the testis was performed by testicular injection of 6-hydroxydopamine (a neurotoxin degenerating sympathetic neural structures) or by vasectomy (cutting the inferior spermatic nerve). If testicular administration of opioid agonist or antagonist was combined with partial denervation of the testis, the effects of pharmacological agents influencing testicular opioid level were not evident. The data indicate that opioid peptides synthesized in the testis are components,of the intratest icular regulatory system and that local opioid actions are modulated by testicular nerves.
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