PubMed Health⌕ Search

Biomedical subjects

A Groppetti

Publications and source records attributed to A Groppetti.

54 records · Page 3Linked to original sources
PubMed1976

Effects of mazindol, a non-phenylethylamine anorexigenic agent, on biogenic amine levels and turnover rate.

1 Mazindol is a new anorexigenic agent which possesses a different chemical structure from that of phenylethylamines, but shows a pharmacological profile similar to that of (+)-amphetamine. 2 Mazindol neither altered whole brain monoamine levels (noradrenaline (NA), dopamine, 5-hydroxytryptamine (5-HT)) nor changed NA levels in the hypothalamus or dopamine levels in the caudate nucleus. 3 Mazindol enhanced dopamine turnover rate in the caudate nucleus, as shown by the increased rate of dopamine decline after blockade of catecholamine synthesis by alpha-methyl-p-tyrosine and decreased the conversion index of (3H)-tyrosine into brain NA. 4 Mazindol administration did not modify pargyline-induced decline of 5-hydroxyindoleacetic acid suggesting that 5-HT turnover is not altered by this drug.

Animals↗
PubMed1975

Effect of hypophysectomy and growth hormone on tryptophan and serotonin metabolism.

The present study reports data on brain serotonin (5-HT) metabolism in two experimental conditions which have in common a lack of pituitary growth hormone (GH) and refers also the effect of a GH replacement therapy. In hypophysectomized female rats or genetically dwarf mice, which have a more selective deficiency of GH, brain tryptophan (TP) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were significantly higher than in age-matched controls. Brain levels of 5-HT were practically unchanged. A GH replacement therapy resulted in both hypophysectomized rats and dwarf mice in a significant reduction of brain TP and 5-HIAA concentrations. These results suggest that GH may exert an inhibitory action on 5-HT metabolism. Consonant with this view are the preliminary findings that in 7 individuals with elevated plasma GH levels for acromegaly, plasma TP levels were lower than in control subjects.

Acromegaly↗
PubMed1972

Effects of amphetamine on the turnover rate of brain catecholamines and motor activity.

1. Rats receiving (+)-amphetamine (either 0.3 or 0.2 mg/kg, i.v.) are anorexic. Only the former dose increases their motor activity. Both doses fail to change dopamine (DM) and noradrenaline (NA) concentrations in striatum and teldiencephalon. The turnover rate of striatal DM is increased only by 0.3 mg/kg of (+)-amphetamine; neither dose changes NA turnover rate in teldiencephalon.2. (-)-Amphetamine (1 mg/kg, i.v.) causes anorexia and hyperthermia in rats but it changes neither the steady-state concentration nor the turnover rate of striatal DM and tel-diencephalic NA. Motor activity is not increased by this dose of (-)-amphetamine.3. Cocaine (3 mg/kg, i.v.) increases motor activity and accelerates the turnover rate of striatal DM. This drug neither accelerates turnover rate of teldiencephalic NA nor causes anorexia.4. These observations suggest that the acceleration of striatal DM turnover rate elicited by (+)-amphetamine and cocaine may be associated with an effect on motor activity. In contrast, the increase of motor activity seems unrelated to the effects of these drugs on noradrenergic tracts of the teldiencephalon.

Animals↗
PubMed1971

Action of fenfluramine on monoamine stores of rat tissues.

1. Fenfluramine is an anorexogenic agent used clinically because it is devoid of central stimulatory effects.2. In rats, fenfluramine causes a depletion of 5-hydroxytryptamine (5-HT) from the telencephalon + diencephalon which lasts longer than one might have expected from the biological half life of fenfluramine. The depleting effects of fenfluramine do not extend to brainstem, stomach and heart stores of 5-HT.3. Fenfluramine causes an increase in the turnover rate of tel-diencephalic 5-HT but such an acceleration could not be detected in the 5-HT stores of the brainstem.4. It is inferred that the effects of fenfluramine on brain 5-hydroxytryptamine may be related to the accumulation of a fenfluramine metabolite in 5-HT neurones.5. High doses of fenfluramine cause a depletion of catecholamine stores in brain and heart but the time course of this depletion is shorter than the depletion of brain 5-HT.

Animals↗
PubMed1969

Lesions of central norepinephrine terminals with 6-OH-dopamine: biochemistry and fine structure.

Intracisternal injections of 6-hydroxydopamine produce rapid and long-lasting depletion of brain catecholamines without effects on serotonin concentrations. Depletion of norepinephrine is greatest in areas containing only nerve terminals and axons and least in areas containing monoamine cell bodies. The norepinephrine loss is accompanied by electron microscopic evidence of nerve terminal degeneration and decreased turnover. Dopamine loss is less marked and is not accompanied by degeneration or alteration of turnover rate.

Animals↗
PubMed1968

Interaction between desipramine, tyramine, and amphetamine at adrenergic neurones.

1. Small doses of tyramine (10 mug/kg intravenously) are taken up by rat heart, which can concentrate the amine 7.3-fold over the plasma level.2. Desipramine (DMI) blocks the uptake of small doses of tyramine by rat heart, but in doses of 20 mg/kg intraperitoneally, it does not affect the cardiac concentrations of tyramine following 20 mg/kg intramuscularly of the drug. The same dose of DMI prevents the depletion of noradrenaline (NA) elicited by intramuscular injection of tyramine 20 mg/kg.3. DMI prevents the depletion of heart NA elicited by (+)-amphetamine 5 mg/kg given intraperitoneally to demedullated rats and enhances the heart concentration of amphetamine.4. Liposoluble amphetamine enters sympathetic nerves by simple diffusion. It is suggested that DMI prevents the release of heart NA caused by this indirect sympathomimetic through an action within the adrenergic neurone.

Amphetamine↗