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Biomedical subjects

A Simonyi

Publications and source records attributed to A Simonyi.

7 recordsLinked to original sources
PubMed1988

Effect of chronic morphine treatment on the adrenaline biosynthesis in adrenals and brain regions of the rat.

Phenylethanolamine-N-methyltransferase (PNMT) activity and tissue catecholamine content were examined after 13 days morphine treatment. Prolonged morphine treatment did not alter the PNMT activity in brain regions (A1/C1 and A2/C2 cell groups, medial basal hypothalamus, median eminence). However, the enzyme activity and the adrenaline content were increased in the adrenal medulla of male rats. In parallel, morphine treatment induced adrenal hypertrophy. In female or hypophysectomized male animals the chronic morphine treatment had no effect on adrenal weight but evoked the increase of PNMT activity. It is concluded that the morphine-induced increased adrenaline biosynthesis in the adrenal gland is not fully dependent on the intact pituitary-adrenal axis and may be mediated partly by a neural mechanism (increased splanchnic nerve activity) or by a direct effect of morphine.

Adrenal Glands↗
PubMed1985

Effect of phenylethanolamine N-methyltransferase inhibition on serum concentrations of luteinizing hormone, follicle stimulating hormone and prolactin in pro-oestrous and ovariectomized rats.

In a dose dependent manner, LY 87130, an inhibitor of adrenaline synthesis in the rat brain, either shifts the pro-oestrous surges of luteinizing hormone and follicle stimulating hormone from the late afternoon to the middle of the night or blocks any occurrence of the surges and prevents ovulation. Because the pulsatile release of LH is also blocked by LY 87130, it is proposed that the role of adrenaline in the production of the preovulatory surge is concerned with the regulation of the LH pulses which constitute the surge.

Animals↗
PubMed1984

Effects of beta-adrenergic inhibitors on noradrenaline and adrenaline metabolism in brain regions of the rat.

Chloranolol (5 mg/kg i.p.) retarded the disappearance of noradrenaline induced by the dopamine-beta-hydroxylase (DBH) inhibitor FLA 63, in the hypothalamus, nucleus of the solitary tract (A-2/C-2 area), and lateral reticular nucleus (A-1/C-1 area) regions, while propranolol (20 mg/kg i.p.) was effective only in the hypothalamus and in the lateral reticular nucleus. The DBH inhibitor-caused accumulation of dopamine was also inhibited by chloranolol in the solitary tract nucleus. Chloranolol and propranolol were able to antagonize the fall in adrenaline concentration due to the phenylethanolamine-N-methyltransferase (PNMT) inhibitor, Lilly 87130, only in the region of the solitary tract nucleus. The data suggest that beta-adrenergic inhibitors reduce noradrenaline and adrenaline turnover in the central nervous system, most characteristically in the solitary tract nucleus and that this effect is possibly related to their antihypertensive effectiveness.

Adrenergic beta-Antagonists↗
PubMed1984

Decrease of morphine-induced prolactin release by a procedure causing prolonged stress.

The effects of morphine and fentanyl on plasma prolactin levels in rats have been measured. It was found that a prolonged immobilization stressful procedure for 5 h inhibited the response to morphine and fentanyl to increase prolactin secretion, but did not influence the increase in plasma prolactin caused by haloperidol. The injection of a large dose of cortisol (25 mg/kg, s.c.) also evoked an inhibition of morphine-induced prolactin release. The inhibition was maximal 24 h after the administration of the glucocorticoid. These results indicate that stress may induce prolonged alteration in endogenous opioid-mediated neuromodulation via a prolonged release of glucocorticoids.

Animals↗
PubMed1983

Long-term ACTH induced diminished responsiveness of prolactin secretion to morphine.

The effect of morphine on plasma prolactin level and on dopamine turnover in the median eminence was studied using adult male rats chronically treated with ACTH. It was found that the ACTH pretreatment caused a decrease in the effect of morphine on prolactin secretion and prevented the inhibitory effect of morphine on dopamine turnover measured in the median eminence. The prolonged ACTH administration did not influence the prolactin content of the pituitaries and the in vitro dopamine sensitivity of lactotroph cells. Acute dexamethasone injection did not change the morphine-caused prolactin release. These results suggest that chronic ACTH treatment (possibly via corticosterone hyperproduction) elicits an opiate-tolerance like state of tuberoinfundibular dopaminergic neurons.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Catalepsy, hypermotility, increase of striatal acetylcholine release induced by morphine and Met-enkephalin as affected by prolonged hydrocortisone and ACTH treatment.

In the rats treated with ACTH or hydrocortisone for 14 days the catalepsy induced by morphine was almost completely inhibited, while the haloperidol induced catalepsy remained unchanged. The morphine induced hypermotility was altered neither by prolonged treatment with ACTH nor by an acute glucocorticoid administration. Inhibition of Na/K ATPase by ouabain led to an increase of striatal acetylcholine (Ach) release, which was enhanced by Met-enkephalin. This effect of the opioid peptide was not demonstrable in the striata of ACTH or hydrocortisone pretreated rats. It is concluded that glucocorticoids are regulatory factors of the striatal opiate neurotransmission possibly via altered receptorial mechanisms.

Adrenocorticotropic Hormone↗