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Biomedical subjects

G Levi

Publications and source records attributed to G Levi.

At least 199 records · Page 11Linked to original sources
PubMed1981

Isolation and physicochemical characterization of electrolectin, a beta-D-galactoside binding lectin from the electric organ of Electrophorus electricus.

Electrolectin, a beta-D-galactoside binding lectin, has been isolated from the electric organ of the electric eel Electrophorus electricus. Electrolectin is purified 1000-fold with a yield of 10 mg/kg of tissue by steps including low speed centrifugation, ammonium sulfate precipitation, and affinity chromatography on a lactosyl-Sepharose column. Electrolectin is a dimer composed of two subunits. The molecular weight of the monomer is around 16,500 as determined by sodium dodecyl sulfate-gel electrophoresis and amino acid analysis. The molecular weight of the dimer determined by equilibrium sedimentation is 32,500 +/- 750. The electrolectin monomer is composed of 144 amino acids and 2.2 +/- 0.45 carbohydrate. It contains one tryptophan but cysteine and metals are absent. The exposure of electrolectin to O2 destroys its hemagglutination activity, abolishes its UV fluorescence and shifts its UV absorption maximum from 287 nm to 250 nm. The oxidation of tryptophan to oxindole is prevented by lactose. The strict requirement of reducing agents for the maintenance of electrolectin agglutination activity is explained by the need to prevent the oxidation of a tryptophan residue in the lactose-binding site. The quantum yields of electrolectin and its complex with lactose are pH dependent and reach a maximal value of 0.4 at neutral pH. The binding constant of lactose to electrolectin is also pH dependent. These data and their temperature dependence stress the important contribution of ionizable groups in the binding of lactose. The latter stabilizes the dimeric structure of electrolectin.

Amino Acids↗
PubMed1981

Enhancement by GABA of glutamate depolarization-induced release from cerebellar nerve endings.

Cerebellar synaptosomes were superfused in the presence of D-[3H]aspartate (to label the glutamate 'reuptake pool') and [14C]glutamine (to label the 'new synthesis pool'). The depolarization-induced release of D-[3H]aspartate and of newly synthesized [14C]glutamate were potentiated by low concentrations of GABA (2--20 microM) or muscimol. The effect was probably mediated by the interaction of GABA with presynaptic GABA receptors localized in 'glutamergic' nerve endings, since it was antagonized by the GABA antagonists picrotoxin and bicuculline.

Animals↗
PubMed1981

Auditory nerve and brain stem responses in homozygous jaundiced Gunn rats.

In humans, functional evidence based on recording cochlear microphonic, auditory nerve, and brain stem responses has shown that the site of lesion in hearing loss following neonatal hyperbilirubinemia is the auditory nerve (with sparing of the hair cells). Structural damage to the central nervous system (CNS) including the cochlear nuclei has been demonstrated in adult, homozygous Gunn rats which develop hyperbilirubinemia shortly after birth. In an attempt to use the Gunn rat as an experimental model for bilirubin-induced CNS damage, auditory nerve and brain stem responses (ABR) were recorded in jaundiced (homozygous) and non-jaundiced (heterozygous) Gunn rats and in Sabra (Wistar) rats. All of the rats including the jaundiced Gunn rats had normal ABR and responded behaviorally to sound stimuli. These results suggest that the adult jaundiced Gunn rat retains auditory function and in this way differs from human patients in whom neonatal jaundice has lead to hearing loss. Therefore, the adult homozygous Gunn rat probably cannot serve as a model for hearing loss due to hyperbilirubinemia.

Animals↗
PubMed1981

Glutamate as a putative transmitter in the cerebellum: stimulation by GABA of glutamic acid release from specific pools.

The aim of the present paper was to determine whether the release of glutamate from putative "glutamergic" terminals in the cerebellum is influenced by gamma-aminobutyric acid (GABA). In a group of preliminary experiments, we present biochemical evidence in favour of a neurotransmitter role of glutamate in the cerebellum: (1) endogenous glutamate was released from depolarized cerebellar synaptosomal preparations in a Ca2+-dependent away; (2) [14C]glutamate was synthesized from [14C]glutamine in cerebellar synaptosomes, and the newly synthesized [14C]glutamate was released released in a Ca2+-dependent way; (3) the elevation of cyclic GMP elicited by depolarization of cerebellar slices in the presence of Ca2+ was partly reversed by the glutamate antagonist glutamic acid diethyl ester, which probably prevented the interaction of endogenously released glutamate with postsynaptic receptors. GABA and muscimol at low concentrations (2--20 micrometers) potentiated the depolarization-induced release of D-[3H]aspartate (a glutamate analogue which labels the glutamate "reuptake pool") from cerebellar synaptosomes. The effect was concentration dependent and was largely prevented by two GABA antagonists, bicuculline and picrotoxin. The stimulation of D-[3H]aspartate release evoked by muscimol was linearly related to the logarithm of K+ concentration in the depolarizing medium. GABA did not affect the overall release of endogenous glutamate, but potentiated, in a picrotoxin-sensitive manner, the depolarization-evoked release of [14C]glutamate previously synthesized from [14C]glutamine. Since nerve endings are the major site of glutamate synthesis from glutamine, GABA and muscimol appear to exert their stimulatory effect at the level of "glutamergic" nerve terminals, probably after interacting with presynaptic GABA receptors. The possible functional significance of these findings is briefly discussed.

Animals↗
PubMed1980

Evidence for a similar compartmentation of recaptured and endogenously synthesized dopamine in striatal synaptosomes.

The aim of the present study was to compare the release pattern of [3H]dopamine ([(3H]DA) originated from [3H]tyrosine or by uptake in striatal synaptosomes. Synaptosomes prelabeled either with [3H]DA or with [3H]tyrosine were superfused in three conditions stimulating DA release by different mechanisms: (1) depolarization with high K+ (2) inversion of the NA+ gradient across the plasma membrane; (3) exposure to d-amphetamine. Since DA contained in different pools may exit from nerve endings by different processes, DA release was analyzed in the presence or in the absence of nomifensine which allows discrimination between carrier-mediated and carrier-independent processes. The pattern of DA release in the three conditions tested was idential, whether [(3)H]DA originated from synthesis or from uptake. Nomifensine did not affect the high-K+-induced release and inhibited that induced by the other two stimuli. The results suggest that newly synthesized and recaptured DA have similar compartmentation in nerve endings.

Animals↗
PubMed1980

A reevaluation of veratridine as a tool for studying the depolarization-induced release of neurotransmitters from nerve endings.

The effect of veratridine on neurotransmitter release was studied using rat brain synaptosomes superfused at 37 degrees C. Veratridine (5-75 microM) caused a concentration-dependent release of [3H]GABA from prelabeled synaptosomes in the presence of 2.7 mM Ca2+. In the whole range of veratridine concentrations, the release of [3H]GABA elicited by the drug was substantially increased rather than decreased in the absence of Ca2+ or with Ca2+ concentrations of 0.45 and 0.9 mM. The release of the amino acid was inhibited more by 5.4 mM than by 2.7 mM Ca2+. The effect on endogenous (chemically measured) GABA was similar to that on [3H]GABA. The inhibitory effect of Ca2+ on the veratridine-induced release of [3H]GABA was consistently seen in a variety of experimental conditions except one, namely when the experiment was run at room temperature (22-23 degrees C) rather than at physiological temperature (37 degrees C). In fact, at 22-23 degrees C the release of GABA evoked by the alkaloid was somewhat potentiated by Ca2+. At 37 degrees C, glutamate appeared to behave similarly to GABA, whereas the veratridine-induced release of [3H]noradrenaline and [3H]dopamaine was largely Ca2+-dependent. The mechanism of the release of transmitters elicited by veratridine is discussed. It is concluded that the evoked release of GABA and glutamate is due more to the veratridine-induced depolarization (Na+ influx) than to the accompanying influx of Ca2+, and it is suggested that the inhibitory effect of Ca2+ on the overall release of amino acids is due to the antagonism exerted by the divalent cation on the veratridine action at the Na+ channel. In contrast, in the case of catecholamines, the influx of Ca2+ would have a prominent role in triggering exocytotic release, whereas the depolarization itself would have slight or no importance.

Animals↗
PubMed1980

Effect of bleomycin on mouse haemopoietic colony forming cells in culture (CFUc).

The kinetics of CFUc studied by hydroxyurea and endotoxin treatments indicate that this cell population is proliferating actively (some 50% in S-phase). This fact implies a peculiar response to (BLM) treatment with Bleomycin, a drug which appears to be proliferation-dependent. The dose-response has a steep initial slope resulting in a low extrapolation number (n = 0.66; D37 = 960 +/- 70 mg BLM/kg body weight). The steep initial slope is confirmed by split-dose experiments resulting in a potentiation effect by fractionation. Further evidence for the dependence of the action of this drug upon the proliferative state of the cell population is derived from time-response studies after single doses of BLM.

Animals↗
PubMed1979

Differential binding of antidepressants to noradrenaline and serotonin transport sites in central nerve endings.

Imipramine and mianserin are equipotent inhibitors of noradrenaline (NA) uptake in synaptosomes. However, after in vivo administration, NA uptake was inhibited only in synaptosomes from imipramine-treated rats, suggesting that imipramine, or its metabolite desipramine, binds to the NA carrier in a manner outlasting the preparation of synaptosomes, whereas mianserin is washed away. To evaluate binding to the NA carrier, synaptosomes prelabeled with 3H-NA were pretreated with an antidepressant and the release of 3H-NA was then stimulated with unlabeled NA. Any reduction of release was taken as an indication of binding. Pretreatment with desipramine, but not with imipramine or mianserin, reduced 3H-NA release suggesting that desipramine is responsible for NA uptake inhibition in synaptosomes from imipramine-treated rats. Transformation of tertiary into secondary amines seems to be crucial for binding to the NA carrier, as confirmed by the stronger binding of nortriptyline and chlordesipramine compared to amitryptiline and chlorimipramine, respectively. In contrast, tertiary amines bound more strongly than secondary amines to the serotonin carrier. Adult and 8-day old synaptosomes showed similar binding properties towards imipramine and desipraine.

Animals↗
PubMed1979

Neurophysiological and neurochemical studies on the action of the anticonvulsant gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide.

The effect of gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide (HEPB) on afterdischarges produced by hippocampal stimulation in cats was studied. HEPB notably diminished the duration of afterdischarges and in some cats blocked their propagation into the substantia nigra and the amygdala. HEPB treatment also antagonized the enhancement of afterdischarge duration produced by subconvulsive doses of bicuculline, whereas treatment with diphenylhydantoin strongly potentiated this effect of bicuculline. The intracisternal injection of HEPB or gamma-aminobutyric acid (GABA) in mice resulted in a potentiation of strychnine-induced convulsions. On the other hand, neurochemical experiments in mouse brain cortex slices and in synaptosomes demonstrated that HEPB did not affect the high affinity uptake of [3H] GABA, its spontaneous or Ca2+ dependent release stimulated by depolarizing K+ concentrations, and its Na+ independent binding to synaptic plasma membranes.

Amygdala↗