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F Nicoletti

Publications and source records attributed to F Nicoletti.

At least 253 records · Page 14Linked to original sources
PubMed1986

Serine-O-phosphate, an endogenous metabolite, inhibits the stimulation of inositol phospholipid hydrolysis elicited by ibotenic acid in rat hippocampal slices.

Serine-O-phosphate (PS) inhibits the accumulation of 3H-inositolmonophosphate elicited by ibotenic acid in rat hippocampal slices incubated in the presence of 7 mM Li+. This inhibition is concentration- dependent and stereoselective, L-PS being 5 fold more potent than D-PS. Among different structural analogues of PS, only L-serine weakly antagonizes the action of ibotenic acid, whereas phosphorylcholine, phosphorylethanolamine and phosphothreonine are inactive even at high concentrations. These results are consistent with the hypothesis that L-PS may act as an endogenous regulator of excitatory amino acid receptor function.

Animals↗
PubMed1986

Excitatory amino acid recognition sites coupled with inositol phospholipid metabolism: developmental changes and interaction with alpha 1-adrenoceptors.

Glutamate, aspartate, ibotenate, and quisqualate activate inositol phospholipid hydrolysis in hippocampal slices prepared from brains of 6- to 8-day-old rats. The stimulation by glutamate and aspartate progressively declines during postnatal development and is negligible after the 24th day of life. In contrast, the stimulation of inositol phospholipid hydrolysis by norepinephrine is low in hippocampal slices from newborn animals and increases during development, reaching mature values after the 35th day of life. In adult hippocampal slices, the stimulation of inositol phospholipid hydrolysis elicited by norepinephrine is inhibited by glutamate in a concentration-dependent fashion. This inhibition can also be brought about by aspartate, 2-amino-4-phosphonobutanoate, and L-phosphoserine, a product of endogenous phosphatidylserine hydrolysis.

Age Factors↗
PubMed1986

Effect of sulpiride on chronic abstinence syndrome in addicted patients.

A total of 410 patients (342 men and 68 women) addicted to heroin for at least 38 months, with or without previous methadone treatment experience, were treated with sulpiride before the appearance of withdrawal syndrome. The drug was injected intramuscularly in a single administration at a dosage of 600 mg. Successively, sulpiride was injected intramuscularly at a dosage of 200 mg 3 times per day from days 2-21 of hospitalization, and then at a dosage of 100 and 50 mg 3 times per day (days 22-25 and 26-29, respectively). All patients showed a suppression of withdrawal signs and symptoms within 6 days of treatment, as assessed by subjective and objective scores. The effect of sulpiride was compared with that of placebo administered to a control group of 10 heroin addicts. Because prolactin has been shown to reduce the dependence of rats to heroin and the naloxone-precipitated withdrawal syndrome in morphine-addicted animals, the effects of sulpiride on heroin addiction may be related to the hyperprolactinemic action of this drug.

Adolescent↗
PubMed1986

Coupling of inositol phospholipid metabolism with excitatory amino acid recognition sites in rat hippocampus.

Ibotenate, a rigid structural analogue of glutamate, markedly enhances the hydrolysis of membrane inositol phospholipids, as reflected by the stimulation of [3H]inositol monophosphate formation in rat hippocampal slices prelabeled with [3H]inositol and treated with Li+. Quisqualate, homocysteate, L-glutamate, and L-aspartate also induce a significant (albeit weaker) increase in [3H]inositol monophosphate formation, whereas N-methyl-D-aspartate, kainate, quinolinate, and N-acetylaspartylglutamate are inactive. The increase in [3H]inositol monophosphate formation elicited by the above-mentioned excitatory amino acids is potently and selectively antagonized by DL-2-amino-4-phosphonobutyric acid, a dicarboxylic amino acid receptor antagonist. These results suggest that, in the hippocampus, a class of dicarboxylic amino acid recognition sites is coupled with phospholipase C, the enzyme that catalyzes the hydrolysis of membrane inositol phospholipids.

Animals↗
PubMed1986

Abnormality of alpha 1-adrenergic receptors in the frontal cortex of epileptic rats.

We found that the binding of [3H]prazosin, a selective ligand for alpha 1-adrenergic recognition sites, is significantly lower in the frontal cortex of the genetically epilepsy-prone rats (GEPRs), as compared with normal Sprague-Dawley rats. Scatchard analysis reveals a decrease in the Bmax of [3H]prazosin binding with no change in the apparent KD, suggesting that there are fewer alpha 1-adrenergic recognition sites in the frontal cortex of the GEPR. This abnormality is associated with a reduced capacity of norepinephrine (NE) to stimulate [3H]inositol monophosphate ([3H]IP1) formation in frontal cortex slices prelabeled with [3H]inositol. No significant differences in [3H]prazosin binding as well as NE-stimulated [3H]IP1 formation have been observed in other brain regions including hippocampus, corpus striatum, and inferior colliculus. These results indicate that a deficit in the alpha 1-adrenergic receptor system in the frontal cortex may play a role in the seizure process in the GEPR.

Animals↗
PubMed1986

The activation of inositol phospholipid metabolism as a signal-transducing system for excitatory amino acids in primary cultures of cerebellar granule cells.

L-Glutamic, L-aspartic acids and a number of their structural analogs, including quisqualic, kainic, ibotenic, quinolinic, and N-methyl-D-aspartic (NMDA) acids, increase inositol phospholipid hydrolysis when added to primary cultures of cerebellar granule cells, as is reflected by an enhanced formation of 3H-inositolmonophosphate (3H-IP1) in the presence of Li+. L-Glutamic acid also enhances the formation of the initial products of inositol phospholipid hydrolysis, 3H-inositol di-(3H-IP2) and triphosphate (3H-IP3). In the absence of extracellular Ca2+, L-glutamic acid fails to enhance 3H-IP1 formation, but still increases 3H-IP2 and 3H-IP3 formation. The stimulation of 3H-IP1 formation elicited by L-glutamic acid is reduced by DL-2-amino-5-phosphonovaleric acid (APV) and gamma-glutamylglycine and, to a lesser extent, by 2,3-cis-piperidindicarboxylic acid (PDA). The stimulation of 3H-IP1 formation by kainic acid is antagonized by PDA and gamma-glutamylglycine, but it is almost unaffected by APV. The increase in 3H-IP1 formation elicited by quisqualic acid is not reduced by any of the dicarboxylic amino acid receptor antagonists that we have tested. We conclude that different subtypes of excitatory amino acid recognition sites are associated with inositol phospholipid metabolism in primary cultures of cerebellar granule cells.

Amino Acids↗
PubMed1985

Estrogen effects on nigral glutamic acid decarboxylase activity: a possible role for catecholestrogen.

Repeated but not single injections of estradiol benzoate significantly reduced nigral glutamic acid decarboxylase (GAD, EC 4.1.1.15). A single injection of the catecholestrogen 2-hydroxyestradiol produced similar results. Tolerance developed to the latter effect, as reflected by the lack of nigral GAD activity changes in rats repeatedly injected with 2-hydroxyestradiol. Repeated injection of the antiestrogen tamoxifen not only failed to antagonize the action of estradiol benzoate but itself reduced nigral GAD activity. Hypophysectomy, which itself decreased nigral GAD activity prevented the lowering effects of either repeated estradiol benzoate administration or single 2-hydroxyestradiol injection on the enzymatic activity.

Animals↗
PubMed1985

Estradiol benzoate decreases nigral GABAergic activity in male rats.

Repeated doses of estradiol benzoate (10 micrograms/kg, s.c., once a day for 2, 5 or 8 days) to male rats decreased gamma-aminobutyric acid (GABA) content and glutamate decarboxylase (GAD) activity in substantia nigra (SN) but failed to change these parameters in hippocampus, cerebral cortex, cerebellum, lateral septum and olfactory tubercle. In the caudate nucleus, estradiol benzoate decreased GABA concentration but did not modify GAD activity. A decrease in nigral GABA concentration and GAD activity was also observed 24 and 48 but not 3 h after a single injection of estradiol benzoate. These data are consistent with results on GAD activity reported by McGinnis et al. in ovariectomized rats. Kinetic analysis of nigral GAD activity revealed that repeated estradiol benzoate injection reduced the Vmax without affecting the Km of GAD. Estradiol benzoate also reduced the rate of nigral GABA accumulation resulting from local infusion of gabaculine, suggesting that the steroid decreases GABA turnover in male rat SN. Hypophysectomy decreased GABA content and GAD activity in SN and GABA content in striatum. Administration of estradiol benzoate for 8 days to hypophysectomized rats failed to decrease further these parameters. Taken together, these data suggest that estradiol benzoate decreases SN GABAergic activity and that the integrity of the pituitary gland is required for this effect.

Animals↗
PubMed1985

Different coupling of excitatory amino acid receptors with Ca2+ channels in primary cultures of cerebellar granule cells.

Cerebellar granule cells in primary culture express receptors for excitatory amino acids. The activation of these receptors results in an increased uptake of Ca2+, however, the effects are different depending on the agonists used. Aspartate, NMDA and ibotenate are active only in depolarized conditions, whereas kainate and glutamate activate Ca2+ uptake independently from depolarization. The results indicate the presence of two receptor types: kainate recognition site coupled with voltage-independent Ca2+ channels and NMDA recognition site coupled with voltage-dependent Ca2+ channels.

Amino Acids↗
PubMed1985

Effects of repeated administration of estradiol benzoate on tubero-infundibular GABAergic activity in male rats.

Repeated (once a day for 8 days) but not single administration of estradiol benzoate (10 micrograms/kg, s.c.) induced a sevenfold increase in anterior pituitary gamma-aminobutyric acid (GABA) concentration in male rats. GABA concentration also increased in the median eminence whereas no changes or decreases were observed in other brain regions including hypothalamic arcuate nucleus, lateral septum, hippocampus, caudate nucleus, and substantia nigra. Eight-day estradiol benzoate injection also enhanced the Vmax of median eminence glutamate decarboxylase activity without affecting the Km of the enzyme for glutamic acid. Taken together, these results suggest that repeated administration of estradiol benzoate increases the activity of the tubero-infundibular GABAergic system in male rats.

Animals↗
PubMed1985

Generalized and focal dystonic syndromes: possible therapy with salmon calcitonin.

We report that repeated administration of salmon calcitonin (20-40 micrograms daily for 30 days) improves dystonic symptoms in patients affected by idiopathic torsion dystonia, blepharospasm-oromandibular dystonia syndrome or writer's cramp syndrome. These results support the suggestion that calcitonin may act at central level influencing the extrapyramidal motor system.

Adolescent↗