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Biomedical subjects

G Levi

Publications and source records attributed to G Levi.

At least 217 records · Page 12Linked to original sources
PubMed1978

Modulation of gamma-aminobutyric acid transport in nerve endings: role of extracellular gamma-aminobutyric acid and of cationic fluxes.

The aim of the present study was to elucidate the possible functional significance of gamma-aminobutyric acid (GABA) homoexchange at nerve endings. Using synaptosomes from adult rat cerebrum, we found that a number of conditions altering cationic fluxes produced a concomitant change in the stoichiometry of GABA homoexchange, In fact, exogenous GABA (10 muM), while not causing net release of intrasynaptosomal GABA in standard conditions, triggered a large net GABA release in the presence of veratridine, Na(+)-K(+)-ATPase inhibitors, or the ionophore A23187, superimposed on that due to the various agents tested alone. This extra release was mediated by the membrane carrier, being largely inhibited by the GABA carrier-blocker L-diaminobutyric acid. The altered stoichiometry of GABA homoexchange observed under these conditions (efflux > influx) appeared to be coupled to the influx of Na(+) (or of Ca(2+)), rather than determined by the establishment of a high intrasynaptosomal [Na(+)]. Under conditions of reversed Na(+) flux (Na(+) efflux), the GABA outward/inward flux ratio was also reversed, and the stoichiometry of GABA homoexchange was in favor of net influx. The possible contribution of K(+) to the effects observed is also discussed. It is concluded that the GABA transport system of nerve endings is susceptible to fine modulation by changes in cationic fluxes similar to those occurring in vivo during depolarization and repolarization. These fluxes may have a prominent role in determining the direction of net GABA transport in GABA-ergic nerve terminals of the living brain.

Aminobutyrates↗
PubMed1978

Release of dopamine from striatal synaptosomes.

The mechanisms of dopamine (DA) release central nerve endings have been investigated utilizing superfused rat striatal synaptosomes. Nomifensine was selected as a tool to discriminate between release mediated by the DA carrier and release occurring independently of the carrier. The following conclusions can be drawn from the results obtained: 1) Alterations of the sodium gradient across the synaptosomal membrane, induced by omission of extracellular Na+ or by ouabain, enhanced the release of 3H-DA from prelabeled synaptosomes. The release was blocked by nomifensine and therefore it was carrier-mediated. 2) The release of DA elicited by amphetamine and related phenylethylamines was nomifensine-sensitive, suggesting that the released DA existed from synaptosomes through the membrane carrier. 3) Depolarization of synaptosomes by high K+ triggered the release of both "newly taken up" and "newly synthesized" DA. 4) The calcium-dependent release of DA (induced by high K+, veratridine of by the ionophore A23187) was not affected by the carrier blocker nomifensine and may occur by an exocytic-like process. 5) The effects of apomorphine and neuroleptics on the stimulus-evoked release of DA do not support the existence of a presynaptic receptor-mediated inhibitory control of DA release identical to that described for noradrenaline.

Animals↗
PubMed1977

Effect of sympathomimetic amines on the synaptosomal transport of noradrenaline, dopamine and 5-hydroxytryptamine.

The interaction of sympathomimetic amines with the transport of 3H-noradrenaline (3H-NE), 3H-dopamine (3H-DA) and 3H-5-hydroxytryptamine (3H-5-HT) were investigated in rat hypothalamic (3H-NE) and striatal (3H-DA) and 3 H-5-HT) synaptosomes. Modifications in the phenylethylamine structure led to changes in activity towards biogenic amine uptake and release: (a) the introduction of a beta-OH group led to compounds less active in inhibiting uptake and stimulating release of 3H-NE, 3H-DA and 3H-5-HT, with the exception of 3H-NE release which was stimulated more by unlabeled 1-NE than by DA; (b) the introduction of phenolic-OH groups always led to compounds which were stronger uptake inhibitors and releasers of the three biogenic amines; (c) the alpha-methylation increased the potency towards uptake inhibition and release stimulation, with the exception of 3H-NE release: in fact, the releasing activity of phenylethylamine was suppressed by alpha-methylation; (d) the introduction of a -Cl group in the para position selectively potentiated the effects on 3H-5-HT uptake and release and generally depressed those on catecholamine transport.

Animals↗
PubMed1976

Decrease of uptake and exchange of neurotransmitter amino acids after depletion of their synaptosomal pools.

Synaptosomes prelabeled at 37 degrees C with radioactive amino acids (GABA, glutamate, glycine, taurine, alpha-aminoisobutyric acid, phenylalanine, leucine) and then washed at 0 degrees C on Millipore filters (DAWP 02500) lost 60-70% of the accumulated radioactivity. The loss was similar with exogenous tritiated GABA and glutamate, and with [14C]GABA and [14C]glutamate metabolically derived from [14C]glucose. In contrast, radioactive norepinephrine, dopamine and 5-hydroxytryptamine were almost totally retained by cold shocked synaptosomes. After pretreatment with reserpine and nialamide the loss of norepinephrine became significantly greater (about 25%). The uptake of radioactive GABA, glutamate and clycine after cold shock was about 50% reduced, whereas that of radioactive biogenic amines was less affected (reduction of 22% for norepinephrine, 29% for 5-hydroxytryptamine and 35% for dopamine). The loss of amino acids and the reduction of uptake could be minimized by performing the cold shock in hypertonic conditions. In synaptosomes prelabeled with [3H]GABA, a good correlation was observed among magnitude of amino acid pool depletion induced by cold shock or by 56 mM KCl, decrease of subsequent accumulation of [14C]GABA, and decrease of [14C]-GABA-stimulated [3H]GABA release (homoexchange).

Amino Acids↗
PubMed1976

Psychopathologic problems in twins during childhood.

Some psychopathologic problems occurring during childhood in twins are discussed from the point of view of mental health. On the basis of case history of twins affected by neurologic or psychiatric disorders some typical situations have been examined: (1) psychopathologic problems arising from perinatal death of the cotwin; (2) psychopathologic problems arising from the death of the cotwin during late childhood; (3) psychopathologic problems arising in the pair from organic or neuropsychaitric event in one of the twins; (4) psychopathologic problems of the twins due to disorders of personal identity and the interaction between the twins. The cases are analyzed from a psychodynamic point of view, in relation to the development of personality in the twins, and from a psychosocial point of view, in relation to the cultural stereotype of the twins during the socialization process and in the context of parental dynamics.

Adolescent↗
PubMed1975

d-Amphetamine as a releaser or reuptake inhibitor of biogenic amines in synaptosomes.

The effect of d-amphetamine on the release of tritiated norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) was analyzed in synaptosomes from different brain area. 3H-NE release was unaffected in the hypothalamus, a region which is rich in noradrenergic terminals, and in cerebellum and pons-medulla, but was substantially increased in corpus striatum and moderately in cerebral cortex. 3H-DA release was strongly enhanced in corpus striatum, a region rich in dopaminergic terminals, substantially increased in cerebral cortex, and slightly increased in the hypothalamus. Since the regional pattern of d-amphetamine-stimulated release was similar with the two catecholamines, but the stimulation was greater with 3H-DA than with 3H-NE, and was more evident in areas richer in dopaminergic terminals, it is suggested that the drug can release 3H-DA or artificially stored 3H-NE from dopaminergic terminals, but not 3H-NE, from noradrenergic terminals. d-Amphetamine also seems capable of releasing 3H-5-HT from serotoninergic terminals. In contrast with the two catecholamines, 3H-5-HT release was more enhanced in cerebral cortex than in corpus striatum.

Animals↗
PubMed1975

Effects of bleomycin on mouse bone-marrow stem cells.

The mouse hematopoietic stem-cell population was tested by the spleen colony technique for effects of the antineoplastic agent bleomycin (BLM). The time response of normal bone marrow was investigated by a single dose of BLM (400 mg/kg) between 0 and 72 hours. The dose response was studied over a wide range of doses (from 40 to 1,600 mg/kg) at a 4-hour exposure. Additional experiments concerned 1) the fraction of colony-forming units in the S phase after BLM administration (by means of pulse hydroxyurea treatment), 2) the response of bone marrow stimulated by endotoxin, and 3) the effects of split-dose treatments. The relatively low toxicity of BLM on both the differentiated and stem-cell populations of unstimulated bone marrow was confirmed and detailed. This drug exhibited peculiar, proliferation-dependent cell inactivation kinetics. Furthermore, BLM induced parasynchronous behavior in the unstimulated stem-cell population. The various aspects of BLM action are discussed with regard to its use in cancer chemotherapy.

Animals↗