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Biomedical subjects

R Invernizzi

Publications and source records attributed to R Invernizzi.

At least 109 records · Page 6Linked to original sources
PubMed1984

Evidence of serotonin involvement in the effect of morphine on dopamine metabolism in the rat nucleus accumbens but not in the striatum.

Morphine-induced increase of dopamine metabolism in the striatum and nucleus accumbens was studied in rats treated with parachlorophenylalanine, an inhibitor of serotonin synthesis, or metergoline and mianserin, two serotonin antagonists. Morphine's effect in the nucleus accumbens, but not in the striatum, was significantly reduced by all the agents used to reduce serotonin transmission. It thus appears that part of the effect of morphine on dopamine metabolism in the nucleus accumbens is mediated by its ability to activate 5-HT function in this area.

Animals↗
PubMed1983

Morphological, cytochemical and ultrastructural studies of a case of systemic mastocytosis.

Morphological, cytochemical and ultrastructural studies of mast cells were carried out in a patient affected with systemic mastocytosis. Neoplastic mast cells showed morphological features between classic tissue mast cells and circulating basophils. They showed strong granule metachromasia after toluidine blue, faint positivity to Hotchkiss reaction, strong positivity to chloroacetate esterase, while they were negative to alkaline phosphatase. Ultrastructural observations showed heterogeneity of granules, most of which had homogenous fine dotted contents. The origin and linkage between mast cells and circulating basophils are discussed.

Alkaline Phosphatase↗
PubMed1982

Is receptor activation involved in the mechanism by which (+)-fenfluramine and (+)-norfenfluramine deplete 5-hydroxytryptamine in the rat brain?

1 The effects of (+)-fenfluramine, (+)-norfenfluramine and reserpine on the concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in brainstem and telencephalon were studied in rats treated with methergoline, a 5-HT antagonist. 2 Methergoline significantly reduced the effect of (+)-norfenfluramine (5 mg/kg) on 5-HT levels in telencephalon and brainstem but did not modify the effect of (+)-norfenfluramine (2.5 mg/kg). 3 Neither the effect of (+)-fenfluramine on 5-HT levels nor the decrease of 5-HT metabolism caused by (+)-fenfluramine and (+)-norfenfluramine was significantly modified by methergoline treatment. 4 Methergoline potentiated the effects of reserpine on brain indoles. The effects was particularly evident on 5-HIAA levels in the brainstem, although significant effects were found on 5-HT in the brainstem and 5-HIAA in the telencephalon depending on the dose reserpine used. 5 The results show that postsynaptic receptor activation may partially contribute to the depletion of brain 5-HT caused by (+)-norfenfluramine in the rat. This mechanism does not seem to play a significant role in the effect of (+)-fenfluramine.

Animals↗
PubMed1981

N-acetyl-beta-glucosaminidase activity in normal and acute leukemia blood cells.

N-acetyl-beta-glucosaminidase activity was studied by cytochemical means in blood cells of 20 normal controls and in blast cells of 21 cases of acute leukemia. All normal granulocytes and monocytes showed finely granular positivity, whereas the lymphocytes were unreactive or showed various granular positivity patterns. The intensity of enzymic activity was not significantly different in the various subtypes of acute leukemia. However the lymphoblasts showed a characteristic positivity pattern with activity being present both in coarse and fine granules located at one pole of the cell. This allowed them to be distinguished from the other leukemic blasts showing fine granules scattered throughout cytoplasm.

Acetylglucosaminidase↗
PubMed1980

Further studies on the mechanism of serotonin-dependent anorexia in rats.

4-(3-Indolyl-2-ethyl) piperidine (LM 5008), 2-(1-piperazinyl) quinoline (quipazine), and metachlorophenylpiperazine (mCPP) were studied for their ability to affect serotonergic mechanisms in vitro. Their relative potency in inhibiting serotonin (5-HT) uptake in vivo and reducing food intake in rats was also examined. mCPP was very potent in displacing 3H-5-HT bound to brain membranes (IC50, 6.2 X 10(-7) M), followed by quipazine, which showed an IC50 of 3.8 X 10(-6) M. LM 5008 was the least effective with an IC50 of 3.6 X 10(-5) M. mCPP and quipazine were less potent than d-fenfluramine in releasing 14C-5-HT from brain synaptosomes, while LM 5008 caused no significant effects at a concentration of 10(-5) M. Conversely, both in vitro and in vivo studies on 5-HT uptake showed that LM 5008 was the most potent compound in inhibiting 5-HT uptake and mCPP the least potent. Since a 50% reduction of food intake was not reached even with a dose of LM 5008 27-times higher than the ED50 for inhibiting 5-HT uptake in vivo, it is suggested that even marked inhibition of 5-HT uptake at central synapses is not sufficient per se to trigger serotonin-dependent anorexia in the rat. Increased release and/or direct stimulation of post-synaptic receptors may be necessary to obtain this effect. This could be of interest for developing new agents which can cause anorexia by interacting with brain serotonin.

Animals↗