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S Amoroso

Publications and source records attributed to S Amoroso.

At least 37 records · Page 2Linked to original sources
PubMed1995

The dorsal noradrenergic bundle modulates DNA remodeling in the rat brain upon exposure to a spatial novelty.

A series of experiments were designed to study the role of the dorsal noradrenergic bundle (DNB) in the modulation of genomic remodeling in the mammalian brain. A series of experiments were designed to study the role of the dorsal noradrenergic system in relation to nonassociative tasks. Adult male Sprague-Dawley rats were either bilaterally lesioned in the DNB by intrabundle microinjection of 6-hydroxydopamine or were sham lesioned. All rats were given 50 microCi [3H-methyl]-thymidine and were sacrificed 0.5 h later. After the injection of the tracer, rats were either left undisturbed in the home cage or were exposed to a Làt-maze for 15 min after 15 min had passed from the time of injection. During the exposure to the maze, corner crossings and rearings were monitored. The rate of DNA synthesis was determined in several brain regions by measuring the amount of tracer incorporated into the DNA over a 0.5-h duration pulse. Under baseline conditions DNB-lesioned rats showed an increase in DNA synthesis in the hippocampus, hypothalamus, and rest of the brain. On the other hand, following exposure to the Làt-maze, sham-lesioned rats only showed an increase in DNA synthesis in the hippocampus, as compared to baseline conditions. Conversely, DNB-lesioned rats did not show an increase in hippocampal DNA synthesis as in the sham-lesioned rats. In contrast, DNA synthesis was increased in the neocortex and rest of the brain. In conclusion, the data support a role for noradrenergic systems in modulating brain DNA synthesis, probably of the unscheduled type, during information processing and storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Adrenergic receptor systems and unscheduled DNA synthesis in the rat brain.

Two experiments were carried out in the albino rat to investigate the role of brain adrenergic systems in DNA remodeling. Adult male Sprague-Dawley rats were given an intraventricular microinjection of an adrenergic drug or vehicle followed 2 h later by the intraventricular injection of 50 microCi of [3H-methyl]thymidine. The rats were sacrificed 0.5 h after the injection of the radioactive tracer. The rate of DNA synthesis was determined by measuring the amount of radioactive precursor incorporated into the DNA extracted from homogenates of several brain areas. In Experiment 1, at time 0 rats received the alpha-adrenergic antagonist phentolamine (5 micrograms), the beta antagonist propranolol (10 micrograms), the alpha agonist phenylephrine (1 microgram), the beta agonist isoproterenol (12.5 micrograms), or the vehicle. The latter decreased UBDS in neocortex, and increased it in the septum, neostriatum, hypothalamus, cerebellum, and rest of the brain. The alpha and beta agonists and antagonists induced several significant effects, depending on the brain region. In Experiment 2, rats were bilaterally lesioned in the dorsal noradrenergic bundle (DNB) by injection of 6-hydroxydopamine or were sham lesioned. One week later, at time 0 they were given the alpha agonist phenylephrine (1 microgram), the beta agonist isoproterenol (12.5 micrograms), or the vehicle. The DNB-lesioned rats showed a higher UBDS in the hippocampus, neocortex, and hypothalamus, which was reversed by the alpha or the beta agonist. The results suggest an influence of the DNB, probably as a tonic inhibitor of UBDS in the hippocampus and the hypothalamus which, in turn, are likely to be mediated by beta- and alpha-adrenergic receptors. In addition, a phasic inhibitory effect seems to be mediated by beta and alpha receptors in the neocortex, and by beta receptors in the cerebellum. A modulatory role of central adrenergic systems on unscheduled brain DNA synthesis may be inferred from these findings.

Afferent Pathways↗
PubMed1994

[The immune changes in the patient with obstructive jaundice: their onset and reversibility after drainage].

Several clinical and experimental studies have demonstrated that the high incidence of septic complications and the high mortality of surgery and invasive diagnostic and therapeutic procedures (ERCP and PTC) in obstructive jaundiced patients are mostly secondary to immune impairment (deficit of Kupffer's cells phagocytic activity and of cell-mediated immunity). The fundamental role of endotoxaemia, that's tightly related to stopped defluxion of biliary salts into the bowel, with bacterial flora increase and secondary passage of germs and toxins into portal and systemic circulation, has recently been demonstrated in the pathogenesis of the main homeostatic alterations in cholestasis (immunodeficiency, disorders of coagulation and renal functionality). This pathogenetic hypothesis explains not only high morbidity and mortality rates, but also the failures of external biliary drainage. The only treatment able to oppose endotoxaemia is internal biliary drainage, endoscopic or percutaneous. These techniques allow the defluxion of biliary salts into the bowel and a relatively quick restore of homeostasis. The authors after having treated high-risk jaundiced patients with internal endoscopic biliary drainage and surgical treatment (after 20-30 days), report excellent results.

Adult↗
PubMed1993

ATP-modulated K+ channels sensitive to antidiabetic sulfonylureas are present in adenohypophysis and are involved in growth hormone release.

The adenohypophysis contains high-affinity binding sites for antidiabetic sulfonylureas that are specific blockers of ATP-sensitive K+ channels. The binding protein has a M(r) of 145,000 +/- 5000. The presence of ATP-sensitive K+ channels (26 pS) has been demonstrated by electrophysiological techniques. Intracellular perfusion of adenohypophysis cells with an ATP-free medium to activate ATP-sensitive K+ channels induces a large hyperpolarization (approximately 30 mV) that is antagonized by antidiabetic sulfonylureas. Diazoxide opens ATP-sensitive K+ channels in adenohypophysis cells as it does in pancreatic beta cells and also induces a hyperpolarization (approximately 30 mV) that is also suppressed by antidiabetic sulfonylureas. As in pancreatic beta cells, glucose and antidiabetic sulfonylureas depolarize the adenohypophysis cells and thereby indirectly increase Ca2+ influx through L-type Ca2+ channels. The K+ channel opener diazoxide has an opposite effect. Opening ATP-sensitive K+ channels inhibits growth hormone secretion and this inhibition is eliminated by antidiabetic sulfonylureas.

Adenosine Diphosphate↗
PubMed1993

Inhibition of the Na(+)-Ca++ exchanger enhances anoxia and glucopenia-induced [3H]aspartate release in hippocampal slices.

The aim of the present study was to investigate the possible role played by the Na(+)-Ca++ exchange system in the modulation of D-[3H]aspartate release induced by anoxia and glucopenia from hippocampal slices. When hippocampal slices were exposed to anoxic and glucopenic conditions (oligomycin + 2-deoxyglucose or 95% N2/5% CO2), an increase of basal D-[3H]aspartate release occurred. Two organic calcium entry blockers, verapamil and nimodipine, and the inorganic calcium entry blocker, gadolinium, did not prevent anoxia-induced D-[3H]aspartate release. In contrast, the calcium-chelator, EGTA, and lanthanum, an inorganic compound that blocks voltage-sensitive calcium channels and Na(+)-Ca++ exchanger activity, enhanced anoxia-induced D-[3H]aspartate release. In addition, the 2'-4'-dimethylbenzil amiloride derivative, a rather specific inhibitor of the Na(+)-Ca++ exchanger system, enhanced anoxia-induced D-[3H]aspartate release. Finally, tetrodotoxin, which selectively blocks the Na(+)-channels, attenuated anoxia-elicited D-[3H]aspartate release. In conclusion, the results of the present study confirmed that, under anoxic and glucopenic conditions, D-[3H]aspartate release was not dependent on the entrance of extracellular Ca++ ions through the voltage-sensitive calcium channels and demonstrated that the inhibition of the Na(+)-Ca++ antiporter enhanced excitatory amino acid release. This result seems to suggest that, when intracellular Na+ concentrations increase, because of the anoxic and glucopenic conditions, both the Na(+)-Ca++ exchanger and the Na(+)-syntransporter system of glutamate operate as Na+ ion efflux pathways. Therefore, when the antiporter is blocked, the syntransporter remains the only pathway for Na+ ion extrusion, leading to an enhancement of D-[3H]aspartate release.

Amiloride↗
PubMed1992

The Na(+)-Ca2+ exchanger activity in cerebrocortical nerve endings is reduced in old compared to young and mature rats when it operates as a Ca2+ influx or efflux pathway.

The activity of the Na(+)-Ca2+ exchanger, which regulates the entry and the extrusion of Ca2+ ions from nerve endings was investigated in Percoll-purified cerebrocortical synaptosomes of aged rats. 45Ca2+ uptake in a Na(+)-free medium and 45Ca2+ efflux in a 145 mM Na+ medium were significantly reduced in cerebrocortical synaptosomes from aged rats (24 months) as compared to those occurring in young (4 months) and mature (14 months) rats. 45Ca2+ influx induced by 55 mM K+, a concentration of K+ ions which selectively promotes Ca2+ entry through voltage-sensitive Ca2+ channels (VSCC), was significantly reduced in mature and aged rats as compared to that occurring in young rats. The impairment of these mechanisms in aged rats is not accompanied by any variation of fura-2 monitored Ca2+ levels under resting and depolarizing conditions.

Animals↗
PubMed1991

[Synchronous carcinoma of the colorectum].

The incidence of synchronous carcinoma of the large intestine is rising in relation to a greater oncogenic environmental charge and increased average life expectancy. There is also a constant risk of not recognising the disease, especially in the case of small carcinoma and, to a greater extent, in patients operated during the occlusive phase. Having underlined the diagnostic value of a correct preparation of the colon prior to instrumental tests, the authors emphasise the importance of a careful intraoperative exploration of the viscera, its preliminary confinement in occluded subjects and repeated surgery in the event of doubts regarding the monolocation of the tumour. Lastly, they underline the importance of postoperative radiological and endoscopic controls since these tests mark both the successful outcome of treatment and the start of follow-up.

Adult↗
PubMed1991

Cytoplasmic alkalinization induced by insulin through an activation of Na(+)-H+ antiporter inhibits tyrosine hydroxylase activity in striatal synaptosomes.

Insulin dose-dependently inhibited tyrosine hydroxylase (TH) activity and increased intrasynaposomal pH (pHi) in rat striatal nerve endings. Both these effects of insulin on TH and pHi were prevented by the 5-(N-methyl-N-(guanidinocarbonylmethyl) amiloride (MGCMA), a putative selective inhibitor of the Na(+)-H+ antiporter. Interestingly when, by changing the extracellular pH (pHo), the pHi was increased, from 7.1 up to 7.5, an equivalent inhibition of TH activity occurred. The inhibitory action exerted from insulin on TH activity disappeared when the hormone was added to synaptosomes whose pHi was lowered to 6.83. Collectively, the results of the present study showed that insulin inhibited TH activity in striatal synaptosomes. This effect seems to involve the activation of the Na(+)-H+ antiporter. This exchange system once activated, may induce an intrasynaptosomal alkalinization, a condition in which TH activity is inhibited.

Amiloride↗
PubMed1990

Glucose, sulfonylureas, and neurotransmitter release: role of ATP-sensitive K+ channels.

Sulfonylurea-sensitive adenosine triphosphate (ATP)-regulated potassium (KATP) channels are present in brain cells and play a role in neurosecretion at nerve terminals. KATP channels in substantia nigra, a brain region that shows high sulfonylurea binding, are inactivated by high glucose concentrations and by antidiabetic sulfonylureas and are activated by ATP depletion and anoxia. KATP channel inhibition leads to activation of gamma-aminobutyric acid (GABA) release, whereas KATP channel activation leads to inhibition of GABA release. These channels may be involved in the response of the brain to hyper- and hypoglycemia (in diabetes) and ischemia or anoxia.

Adenosine Triphosphate↗
PubMed1990

Possible involvement of Ca++ ions, protein kinase C and Na(+)-H+ antiporter in insulin-induced endogenous dopamine release from tuberoinfundibular neurons.

Insulin (63 microM) stimulated endogenous dopamine (DA) release from tuberoinfundibular neurons. This effect was independent on the presence of extracellular glucose and did not involve the outward transport of DA, mediated by its membrane carrier. By contrast this effect was completely prevented by the removal of extracellular Ca++ ions in presence of the Ca(++)-chelator ethyleneglycol-2-(2-aminoethyl)-tetracetic acid (EGTA). Furthermore 1-(5-isoquinolinyl-sulfonyl)-2-methyl-piperazine (H7), a compound which behaves as a putative inhibitor of protein kinase C (PK-C) (10 microM), completely counteracted the stimulation of endogenous DA release induced by insulin. Amiloride (300 microM) and its 5-amino nitrogen atom-substituted derivative, 5-(N-methyl-N-(guanidinocarbonylmethyl) amiloride (MGCMA) (10 microM), a highly selective inhibitor of the Na(+)-H+ membrane antiporter, were both able to prevent the stimulatory action exerted by insulin on endogenous DA release. Collectively, these results suggest that the transductional events by which insulin stimulated endogenous DA release from TIDA neurons may involve the activation of PK-C, the enhancement of Ca++ influx and the stimulation of the Na(+)-H+ exchange system.

Amiloride↗
PubMed1990

K+ channel openers activate brain sulfonylurea-sensitive K+ channels and block neurosecretion.

Vascular K+ channel openers such as cromakalim, nicorandil, and pinacidil potently stimulate 86Rb+ efflux from slices of substantia nigra. This 86Rb+ efflux is blocked by antidiabetic sulfonylureas, which are known to be potent and specific blockers of ATP-regulated K+ channels in pancreatic beta cells, cardiac cells, and smooth muscle cells. K0.5, the half-maximal effect of the enantiomer (-)-cromakalim, is as low as 10 nM, whereas K0.5 for nicorandil is 100 nM. These two compounds appear to have a much higher affinity for nerve cells than for smooth muscle cells. Openers of sulfonylurea-sensitive K+ channels lead to inhibition of gamma-aminobutyric acid release. There is an excellent relationship between potency to activate 86Rb+ efflux and potency to inhibit neurotransmitter release.

Animals↗
PubMed1989

Cobalt-sensitive and dihydropyridine-insensitive stimulation of dopamine release from tuberoinfundibular neurons by high extracellular concentrations of barium ions.

Recently, it has been demonstrated that Ca2+ entrance into the neuronal cytoplasm can occur upon the activation of 3 different types of specific voltage-dependent channels which can be characterized according to the following criteria: (1) voltage threshold for activation; (2) tendency to inactivation; (3) bivalent cation permeability; and (4) drug sensitivity. In this study we investigated, in tuberoinfundibular dopaminergic (TIDA) hypothalamic neurons, the biochemical and pharmacological properties of Ca2+ channels, by comparing the effects of high extracellular concentrations of Ba2+ and Ca2+ ions on [3H]dopamine (DA) release from TIDA neurons. The results obtained show that extracellular Ba2+ ion concentrations dose-dependently (10-20 mM) stimulated [3H]DA release from superfused TIDA neurons and that this effect was prevented by Co2+ ions (2 mM). In addition, superfusion of TIDA neurons with a concentration of Ca2+ ions equimolar to that of Ba2+ ions (20 mM) failed to modify [3H]DA release. The fact that tetraethylammonium (10 mM), a blocker of K+ currents in excitable cells, did not mimick the stimulatory action of Ba2+ ions on [3H]DA release, seems to exclude that the effect of Ba2+ ions was dependent on the inhibition of K+ channels in TIDA neurons. The omission of Ca2+ ions from the extracellular medium did not prevent the stimulatory effect on [3H]DA release elicited by elevated concentrations of Ba2+ ions, but rather reinforced this effect. Finally, nitrendipine (50 microM) did not modify the stimulatory effect of high extracellular Ba2+ ions on [3H]DA release from TIDA neurons.

Animals↗
PubMed1989

Pharmacological characterization of serotonin receptors involved in the control of prolactin secretion.

The present study was undertaken to characterize the type of serotonin (5-HT) receptors involved in the control of prolactin (PRL) secretion in male rats. d-Fenfluramine (10 mg/kg i.p.), a potent 5-HT releaser and quipazine, (20 mg/kg i.p.) a 5-HT agonist, caused a marked increase in serum PRL levels. Ritanserin (200 micrograms/kg i.p.), a specific antagonist of 5-HT2 receptors, administered 1 h before the administration of d-fenfluramine or quipazine, completely prevented the PRL-releasing effect of these drugs. Furthermore, the administration of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH DPAT) (1.5, 3 and 6 mg/kg i.p.), a compound considered to be a prototypical 5-HT1A agonist, failed to induce any change in serum PRL levels. The same lack of effect on PRL secretion was observed after the administration of 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridin-4-yl)-1-H-indole (RU 24969) (1, 3 and 10 mg/kg i.p.), a compound which has been shown to possess a higher selectivity for 5-HT1B receptor subtypes than for 5-HT1A subtypes. These results suggest that 5-HT receptors involved in the control of PRL secretion are of the 5-HT2 type.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Purification of Parj I, a major allergen from Parietaria, judaica pollen.

A major allergen, the Parj I, was purified to homogeneity from Parietaria judaica pollen by means of ultrafiltration dialysis, preparative polyacrylamide gel chromatography and affinity chromatography through a column of Sepharose-monoclonal antibody specific for Parj I. The homogeneity of the Parj I was assessed by one single arc of immunoprecipitation both in cross immunoelectrophoresis (CIE) and crossed radioimmunoelectrophoresis, by one single band of radiostaining after a sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transfer to nitrocellulose and by one single peak after a size exclusion chromatography on high-performance liquid chromatography (HPLC). The homogeneity was further supported by crossed Laurell immunoelectrophoretic analysis, in that only one arc of precipitation was magnified in CIE after addition of the purified allergen. The purified Parj I allergen was capable of interacting in vitro with 70% of the human IgE specific for a crude P. judaica extract, as determined by radioallergosorbent test inhibition. The purified Parj I was capable of inducing positive reactions in vivo in skin prick tests, and of inducing release of histamine from blood containing basophils as determined by a histamine release assay. The amino acid analysis of the Parj I showed 118 amino acid residues per monomer analyzed and, among other residues, three methionine residues were detected. The molecular weight of the Parj I estimated by HPLC and amino acid composition was 26 kilodaltons.

Allergens↗
PubMed1988

Effect of different Ca2+ entry blockers on dopamine-induced inhibition of in vitro prolactin secretion.

The organic Ca2+ entry blockers nimodipine, verapamil, flunarizine and diltiazem belong to different chemical classes but antagonized, at the concentrations of 1 and 10 microM, the inhibitory effect exerted by 1-10 microM dopamine on in vitro prolactin secretion from the pituitary gland. The results suggest a close functional interaction between Ca2+ entry blockers and the dopamine receptors involved in the inhibition of prolactin secretion.

Animals↗
PubMed1988

Evidence for a differential interaction of buprenorphine with opiate receptor subtypes controlling prolactin secretion.

We studied the effects of various doses of the opiate derivative buprenorphine on serum prolactin levels and whether these effects could be counteracted by pretreatment with the opiate receptor blocker naloxone. The administration of increasing doses of buprenorphine exerted a dual effect on serum prolactin levels. At low doses (3, 10 and 30 micrograms/kg) this agent increased serum prolactin levels. This effect disappeared with increasing doses (100 and 300 micrograms/kg), and at the highest doses (1000 and 3000 micrograms/kg) the levels of serum prolactin decreased. Naloxone (30 mg/kg) decreased serum prolactin levels and reversed both the stimulatory and the inhibitory action of buprenorphine. These data are compatible with the hypothesis that buprenorphine could interfere with two different, but inter-dependent receptors: at low doses the oripavine derivative could act at one receptor site to cause an increase of serum prolactin, whereas at higher doses it could interact with a second site of lower affinity that is responsible for the inhibition of prolactin secretion. When buprenorphine (at high doses) activates the lower affinity site, the interaction with this receptor counteracts and reverses the effects of the high affinity site. On the basis of this hypothesis, naloxone should block both receptors.

Animals↗
PubMed1988

Pure uptake blockers of dopamine can reduce prolactin secretion: studies with diclofensine.

The effects of diclofensine, a pure dopamine (DA) uptake inhibitor on 1) 3H-DA uptake in rat arcuate-periventricular nucleus-median eminence synaptosomes, 2) basal and K+-evoked endogenous DA release from tuberoinfundibular dopaminergic (TIDA) neurons and 3) in vivo prolactin (PRL) secretion were studied. Diclofensine, in concentrations of 0.01, 0.1 and 1 microM caused a marked decrease of 3H-DA uptake. In addition, it was unable to stimulate basal endogenous DA release which, on the contrary, was elicited by d-amphetamine in the same concentration (50 microM). On the other hand, diclofensine (50 microM) caused a 3 fold enhancement of K+-evoked DA release. Finally, the compound, when administered in vivo to male rats, significantly reduced basal serum PRL levels. The results of the present study seem to indicate that the pharmacological blockade of DA uptake in TIDA neurons is a condition sufficient to cause a reduction of PRL release.

Animals↗