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Biomedical subjects

G Blanc

Publications and source records attributed to G Blanc.

At least 19 recordsLinked to original sources
PubMed1994

Blockade of prefronto-cortical alpha 1-adrenergic receptors prevents locomotor hyperactivity induced by subcortical D-amphetamine injection.

The stimulation of cortical dopaminergic D1 receptors can counteract the increased locomotor activity evoked by D-amphetamine application in the nucleus accumbens (Vezina et al., Eur. J. Neurosci., 3, 1001-1007, 1991). Moreover, an alpha 1 antagonist, prazosin, prevents the locomotor hyperactivity induced by electrolytic lesions of the ventral tegmental area (Trovero et al., Neuroscience, 47, 69-76, 1992). Attempts were thus made to see whether blockade of alpha 1-adrenergic receptors in the rat prefrontal cortex could reduce nucleus accumbens D-amphetamine-evoked locomotor activity. Rats implanted chronically and bilaterally with cannulae into the medial prefrontal cortex and the nucleus accumbens were used for this purpose and locomotor activity was monitored in circular corridors. Preliminary experiments indicated that intraperitoneal injection of prazosin (0.06 mg/kg) reduces the locomotor hyperactivity induced by the peripheral administration of D-amphetamine (0.75 mg/kg). This effect of prazosin was not observed when locomotor hyperactivity was obtained by an intraperitoneal injection of scopolamine (0.8 mg/kg). Bilateral nucleus accumbens injections of D-amphetamine (4.0 nmol/side) markedly increased locomotor activity, as estimated in a 30 min period. Prior (20 min) bilateral injections of either prazosin or WB-4101 (0.16 pmol) into the medial prefrontal cortex abolished the nucleus accumbens D-amphetamine-evoked response. The recovery of the nucleus accumbens D-amphetamine-evoked response was closely dependent on the amount of prazosin used, very prolonged inhibitory effects of the drug being seen with a high amount (> 4 days with 160 pmol). In contrast, whatever the amount of WB-4101 used (0.16-160 pmol), recovery occurred within 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Blockade of D-1 dopamine receptors in the medial prefrontal cortex produces delayed effects on pre- and postsynaptic indices of dopamine function in the nucleus accumbens.

The present experiments assessed the acute and delayed effects of D-1 dopamine (DA) receptor blockade in the medial prefrontal cortex (mPFC) on pre- and postsynaptic indices of DA neurotransmission in the nucleus accumbens (N.Acc). Different groups of rats received intra-mPFC injections of saline (control animals) or the D-1 DA receptor antagonist SCH-23390 (0.25 microgram/side). Acutely, intra-mPFC injections of this antagonist did not affect spontaneous locomotion but significantly increased the locomotion induced by intra-N.Acc. amphetamine (1.5 micrograms/side), in agreement with our earlier findings [Vezina et al. (1991) Eur. J. Neurosci., 3:1001-1007]. When tested two days post-injection, however, mPFC-SCH-23390 preexposed animals showed lower levels of locomotor activity than Control animals in response to intra-N.Acc. injections of amphetamine. This effect was not observed in other animals preexposed two days earlier to mPFC injections of amphetamine (2.5 micrograms/side) or the D-2 DA receptor antagonist sulpiride (1.0 microgram/side). Animals preexposed two days earlier to mPFC SCH-23390 also showed higher levels of locomotor activity (+98%) when tested with intra-N.Acc. injections of the D-1 DA receptor agonist SKF-38393 (1.0 microgram/side) and a 36% increase in maximal DA-sensitive adenylate cyclase activity in comparison to Control animals. These effects were no longer observed in animals tested seven days following the mPFC SCH-23390 injections. These results demonstrate delayed actions resulting from cortical D-1 DA receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1993

Influence of pancreatic ducts on saturation of juice with calcium carbonate in dogs.

In several species, bicarbonate and calcium concentrations of pancreatic juice are known to vary during the different phases of pancreatic secretion. The effects of these variations on the saturation of juice with calcium carbonate, a critical factor for the formation of pancreatic stones, are not known. In this work, we studied the saturation degree of pancreatic juice with calcium carbonate in six unanesthetized beagle dogs equipped with Thomas cannulae during basal secretion and after bolus injections of cerulein (30 ng/kg) or secretin (0.25 units/kg). In the different samples of pure pancreatic juice, pH, PCO2, bicarbonate, and proteins were measured by standard methods. Total calcium (CaT) and ionized calcium (Ca2+) were determined using calcium-specific electrodes. Saturation with calcium carbonate was calculated by reference to the solubility product of calcite at 37 degrees C. Almost all the samples were found to be supersaturated with calcium carbonate but large variations of the saturation index were observed. In basal samples, obtained during periods of low secretion rate, the mean saturation index (3.35 +/- 3.01) was significantly lower than under secretion (12.10 +/- 5.14) or cerulein (18.01 +/- 8.42). This low basal saturation index, in spite of a high Ca2+ content, was explained by a low bicarbonate concentration (37.6 +/- 18.9 mmol/liter) and a high PCO2 (13.4 +/- 7.5 kPa). In contrast, in juice obtained after hormonal stimulation, PCO2 (4.8 +/- 1.6 kPa) was similar to plasma PCO2 (5.5 +/- 1.2 kPa).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Experimental study of the antibacterial activity of cloth impregnated with a disinfectant solution].

Disinfecting cloths were commercialized for several years. The solutions of disinfectant used are generally active in vitro in the conditions required by the french standards published by AFNOR, but it is also necessary to know the effectiveness of disinfecting cloths in conditions of use. We describe in this paper a method for this determination. Four bacterial stains recommended in the french standards were used: Staphylococcus aureus ATCC 9144, Enterococcus hirae ATCC 10541, Pseudomonas aeruginosa CIP A 22 and Escherichia coli ATCC 10536. The bacteria were layed on a test watch-glass and the disinfecting cloth was applied on it following the conditions recommended by the manufacturer. 15 minutes after using the disinfecting cloth, the bacteria on the watch-glass and those which were recovered on the disinfecting cloth during application were collected in a neutralising agent suitable for the disinfecting solution used and the surviving bacteria were counted. A similar test was performed using cloth impregnated with sterile distilled water. We studied the activity of unweaved cloths impregnated with a mixture of quaternary ammonium compounds (0.5%) and peroxides (0.1%). The results show that the method allows us to estimate the proper activity of the disinfectant used. In this study, a much higher decontamination of the watch-glass was observed with impregnated cloths than with cloths containing distilled water only. The mean reduction of the number of bacteria layed on the watch-glass was 5.95 log10 in 15 minutes in the first case and only 2.4 log10 in the second case. In addition, the disinfectant leads to the destruction of the bacteria recovered on the cloth during application.

Bedding and Linens↗
PubMed1992

Contribution of an alpha 1-adrenergic receptor subtype to the expression of the "ventral tegmental area syndrome".

Bilateral electrolytic lesions of the rat ventral tegmental area, a mesencephalic structure containing the cell bodies of ascending dopaminergic neurons, induce a behavioural syndrome characterized by a permanent locomotor hyperactivity. Acute intraperitoneal injections of prazosin, an alpha 1-adrenergic receptor antagonist, at a dose (0.5 mg/kg) which does not affect locomotor activities of control animals, abolished locomotor hyperactivities of lesioned rats. Antagonists of other monoaminergic receptors (propranolol, ritanserin, yohimbine), and also another antagonist of alpha 1-adrenergic receptors, 2-(2',6'-dimenthoxyphenoxyethyl)-aminomethyl-1,4-benzodioxan (WB4101) were ineffective. Comparisons of autoradiograms of brain slices incubated in the presence of 1 nM [3H]prazosin or 10 nM [3H]WB4101 indicated clear topographical differences. [3H]Prazosin labelling is present in the septum and in layer III of the cerebral cortex but absent in the striatum. [3H]WB 4101 labelling is diffuse in the superficial layers of the cerebral cortex and present in the striatum. In addition, intraperitoneal injection of WB4101 displaces, only weakly, [3H]prazosin binding in layer III of the cerebral cortex (-18%) while it decreases by 50% [3H]prazosin binding in the more superficial cortical layers. These observations strongly suggest that the binding site labelled by [3H]prazosin is different from alpha 1A- and alpha 1B-adrenergic receptor subtypes labelled by [3H]WB4101. Finally, it is proposed that the prazosin-induced blockade of the locomotor hyperactivity exhibited by ventral tegmental area lesioned animals is linked to the previously demonstrated regulatory role of noradrenergic neurons on cortical dopamine transmission.

Adrenergic alpha-Antagonists↗
PubMed1992

Autoradiographic identification of D1 dopamine receptors labelled with [3H]dopamine: distribution, regulation and relationship to coupling.

On the basis of experiments made on striatal membranes, Leff and Creese [Molec. Pharmac. (1985) 27, 184-192] have proposed that tritiated dopamine binds to a high-affinity agonist state of D1 dopamine receptors (D1h) which adopt this conformation when they are associated with the GTP-binding protein involved in the transduction process. Quantitative autoradiography was thus used to look for the distribution of these D1h sites in the rat brain and to compare it with that of D1 receptors labelled with [3H]7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benz aze pine [( 3H]SCH23390), a D1 antagonist. The effects of unilateral 6-hydroxydopamine lesion of the ascending dopamine pathways on the density of [3H]dopamine D1h and [3H]SCH23390 binding sites in the striatum and the nucleus accumbens were also analysed. In the striatum, when D2 receptors were blocked by spiroperidol (20 nM), [3H]dopamine was found to bind specifically to dopamine receptors of the D1 type. Complementary experiments made with dopamine uptake blockers indicated that high-affinity dopamine uptake sites were not labelled by [3H]dopamine under our experimental conditions. The anatomical distribution of [3H]dopamine D1h binding sites was found to be markedly different from that of [3H]SCH23390 binding sites. This was particularly the case in the substantia nigra, some amygdaloid nuclei and the prefrontal cortex--structures in which the ratios between [3H]SCH23390 and [3H]dopamine binding sites were more than seven-fold higher than that observed in the striatum. [3H]SCH23390 binding was not significantly affected in either the striatum or the nucleus accumbens six weeks after a complete unilateral destruction of ascending dopamine pathways. In contrast, a marked decrease in [3H]dopamine D1h binding sites was found in both structures, but this effect was lower in the medioventral (-60%) than in the laterodorsal (-81%) part of the striatum, even though dopamine denervation was uniform throughout the structure. Preincubation of the sections with dopamine (0.5 microM) led to a partial recovery (+126%) in the lesioned striatum and an increase of [3H]dopamine labelling in the control striatum (+68%). This suggest that the presence of dopamine stabilizes the D1h state of D1 receptors. The absence or low amount of dopamine, either due to dopamine denervation or naturally occurring (prefrontal cortex), would then impair the [3H]dopamine D1h binding. In addition, a lower coupling of D1 receptors with adenylate cyclase was observed in the substantia nigra when compared to that in the striatum: this may explain the relatively weak [3H]dopamine binding in the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed1992

Efficacy, safety and acceptability of halofantrine in the treatment of acute Plasmodium falciparum malaria in African children (Gabon).

Halofantrine chlorhydrate 2 per cent suspension was given to 50 children (mean age 6.2 years in a dose of 8 mg/kg three times a day as a single day treatment. The children were born and lived in Gabon, where malaria transmission is continuous. They all had acute Plasmodium falciparum malaria. The children were kept in hospital for 5 days, and regularly followed over a 15-day period. The 50 children were cured and efficacy was evaluated as good in 44 cases, and excellent in six cases, as judged by improvement in their clinical signs and parasitaemia. Two criterias were considered in the evaluation of efficacy: clearance of parasitaemia (mean day 4), fever clearance (mean hour 24). There were two cases of persistences of parasites at day 15 with a very low parasitaemia rate. Tolerance to halofantrine was good from a clinical and biological point of view. Acceptability was excellent in all cases. Halofantrine 2 per cent suspension is a good alternative in the treatment of acute Plasmodium falciparum malaria in children, especially with the present situation of multidrug-resistant strains in Central Africa.

Acute Disease↗
PubMed1992

In vivo partial inactivation of dopamine D1 receptors induces hypersensitivity of cortical dopamine-sensitive adenylate cyclase: permissive role of alpha 1-adrenergic receptors.

As shown by autoradiography, peripheral injections of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) induced a dose-dependent decrease of [3H]SCH 23390 and [3H]prazosin high-affinity binding sites in the rat prefrontal cortex. EEDQ showed similar efficacy in inactivating cortical and striatal dopamine (DA) D1 receptors, whereas prazosin-sensitive alpha 1-adrenergic receptors were more sensitive to the action of the alkylating agent, as for all doses of EEDQ tested (from 0.8 to 3 mg/kg, i.p.), the decrease in cortical [3H]SCH 23390 binding was less pronounced than that of [3H]prazosin. The effects of EEDQ on [3H]SCH 23390 binding and DA-sensitive adenylate cyclase activity were then simultaneously compared in individual rats. In the striatum, whatever the dose of EEDQ used, the decrease of DA-sensitive adenylate cyclase activity was always lower than that of D1 binding sites, suggesting the occurrence of a large proportion of spare D1 receptors. In the prefrontal cortex, a significant increase in DA-sensitive adenylate cyclase activity was observed in rats treated with a low dose of EEDQ (0.8 mg/kg), this effect being associated with a slight reduction in [3H]SCH 23390 binding sites (-20%). Parallel decreases in the enzyme activity and D1 binding sites were observed with higher doses. The EEDQ-induced supersensitivity of DA-sensitive adenylate cyclase did not occur in rats in which the decrease in [3H]prazosin binding sites was higher than 35%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1992

Nicotine and morphine differentially activate brain dopamine in prefrontocortical and subcortical terminal fields: effects of acute and repeated injections.

Acute systemic injections of nicotine and morphine produce increased locomotion and repeating these injections produces an enhanced locomotor effect. Different lines of evidence suggest that both the acute and sensitized locomotion elicited by morphine are linked to activity in the mesolimbic dopamine (DA) system. The present experiments assessed the effect of acute and repeated injections of nicotine on DA utilization [3,4-dihydroxyphenylacetic acid (DOPAC)/DA] in subcortical and prefrontocortical DA terminal fields and compared these to the effects of morphine. Acute nicotine produced substantial increases in the DOPAC/DA ratio in the nucleus accumbens (N. Acc.) and the antero-medial striatum but not in the dorso-lateral striatum or the medial prefrontal cortex (mPFC). Repeated injections greatly reduced or abolished the drug's effects in the first two terminal fields and produced an increase in DA utilization in the mPFC. In contrast, acute morphine produced large increases in the DOPAC/DA ratio in both the N.Acc. and the mPFC. Consistent with previous findings, repeated morphine increased its effects further in the N. Acc. and produced a small decrease in the mPFC. Neither nicotine nor morphine produced changes in baseline DA utilization in any site. Finally, repeated exposure to nicotine did not enhance the locomotor response to a subsequent injection of morphine. These findings suggest that nicotine differs from morphine in the way it elicits locomotion following repeated injection and possibly in its relation to DA as a mediator of reward. They are also consistent with evidence for a functional interaction between the effects of DA in subcortical and prefrontocortical sites.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Different regulations of dopaminergic (D1) receptors and neurotensinergic binding sites in the rat prefrontal cortex.

The effects of the destruction of mixed dopamine/neurotensin (DA/NT) meso-cortical neurons were investigated by studying the development of denervation supersensitivity of DA (D1) and NT cortical post-synaptic binding sites using respectively [3H]SCH 23390 and [125I]NT as ligands. These neurons were destroyed bilaterally either by injection of 6-hydroxydopamine (6-OHDA) or by an electrolytic coagulation made in the ventral tegmental area (VTA). Five weeks later, both [3H]SCH 23390 and [125I]NT bindings were analysed by quantitative autoradiography on each lesioned animal and on corresponding controls. The chemical lesions of the VTA induced an increase in the density of the cortical NT binding sites but did not affect D1 binding sites. On the contrary, electrolytic lesions induced an increase in D1 binding sites and no change in NT binding sites. One possible explanation of these differences may be that, since chemical lesions of the VTA destroy noradrenergic (NA) ascending pathways while electrolytic lesions spare the cortical NA innervation, the observed modifications of D1 and NT cortical binding sites following their presynaptic denervation are dependent on the presence (increase in D1 receptors) or the absence (increase in NT binding sites) of the cortical NA innervation.

Animals↗
PubMed1991

Use of concanavalin A for coating the membranes of stallion spermatozoa.

Semen from three ejaculates from each of 4 stallions was frozen in liquid nitrogen. Morphology was evaluated by coating the spermatozoa with fluorescein-labelled Concanavalin A (FITC-ConA2) and motility was measured by computer-assisted image analysis. Coating was performed at each step of the freezing procedure (dilution, cooling, addition of glycerol and freeze-thawing) and observations were made after each step, to evaluate changes, or after subsequent steps, to determine protection provided by the coating method. All the parameters showed progressive changes during the freezing procedure. Mean track speed of the spermatozoa, the proportions of normal and motile spermatozoa and lateral head displacement all decreased, whereas the proportions of spermatozoa exhibiting non-fluorescence in the equatorial segment and wrinkled acrosome membranes increased. The results demonstrated that coating stallion spermatozoa with ConA2 provides some degree of protection for acrosome membranes and it helps to preserve motility after freezing and subsequent thawing.

Animals↗
PubMed1990

Involvement of dopamine neurons in the regulation of beta-adrenergic receptor sensitivity in rat prefrontal cortex.

The contribution of dopamine (DA) afferents to the regulation of beta-adrenergic receptor sensitivity (isoproterenol-stimulated adenylate cyclase activity) in the rat prefrontal cortex was investigated by comparing the effects of lesions affecting either both DA and noradrenaline (NA) or NA fibers alone. Bilateral 6-hydroxydopamine (6-OHDA) lesions made in the ventral tegmental area destroyed ascending DA and to a variable extent ascending NA fibers innervating the prefrontal cortex. Two opposite effects were observed depending on the extent of cortical NA denervation: (a) When NA denervation was complete (less than 4% of controls), a marked increase in the isoproterenol-sensitive adenylate cyclase activity (+78%) was found. The amplitude of this denervation supersensitivity was similar to that occurring following complete and selective destruction of NA innervation induced by bilateral 6-OHDA injections made into the pedunculus cerebellaris superior. (b) When 6-OHDA injections into the ventral tegmental area led to a partial destruction of cortical NA afferents (10-40% of control values), a hyposensitivity of the isoproterenol-induced adenylate cyclase activity (-30%) was observed. This effect contrasted with the moderate supersensitivity seen in rats with partial, but selective, destruction of NA innervation (pedunculus cerebellaris superior lesions). The hyposensitivity of beta-adrenergic receptors obtained in rats with partial lesions of cortical NA fibers, but devoid of cortical DA innervation, suggests that DA neurons may regulate, under certain conditions, the denervation supersensitivity of beta-adrenergic receptors.

Adenylyl Cyclases↗
PubMed1989

Nondopaminergic prefrontocortical efferent fibers modulate D1 receptor denervation supersensitivity in specific regions of the rat striatum.

A unilateral injection of 6-OHDA (6 microgram/1.5 microliter) was made into the fields of Forel in order to estimate the effects of the destruction of ascending dopaminergic (DA) pathways on the denervation supersensitivity of DA D1 receptors in the rat striatum. DA-sensitive adenylate cyclase activity was markedly enhanced in the anteromedian part of the striatum 3 weeks after the lesion (+68%) and remained elevated for several weeks thereafter (+36%). A different response occurred in the laterodorsal striatum, where the increase in DA-sensitive adenylate cyclase activity was less pronounced after 3 weeks (+40%) and no longer present after 7 weeks. Estimations of catecholamine levels indicated that the lesion made destroyed not only nigrostriatal DA neurons but other ascending catecholaminergic fibers projecting into the cerebral cortex as well. In addition, retrograde transport experiments made with wheat germ agglutinin coupled to horseradish peroxidase indicated that the anteromedian part of the striatum, but not the laterodorsal one, receives both an ipsi- and contralateral cortical projection originating in the prefrontocortical DA field. When the destruction by 6-OHDA of this contralateral DA innervation was combined to the unilateral lesion of the fields of Forel, the increase in DA-sensitive adenylate cyclase activity in each striatal area 3 or 7 weeks postlesion was prevented. This effect was due to DA denervation of the prefrontal cortex since striatal D1 denervation supersensitivity was still observed when contralateral ascending noradrenergic fibers were selectively destroyed by a 6-OHDA lesion made laterally to the pedunculus cerebellaris superior. These results suggest that, by controlling the activity of corticostriatal neurons, the mesocorticoprefrontal DA neurons exert a permissive role on the development of D1-receptor denervation supersensitivity in specific areas of the striatum.

Adenylyl Cyclases↗
PubMed1988

Behavioural deficits induced by an electrolytic lesion of the rat ventral mesencephalic tegmentum are corrected by a superimposed lesion of the dorsal noradrenergic system.

The bilateral electrolytic lesion of the ventral mesencephalic tegmentum (VMT) induces, in the rat, behavioural deficits such as locomotor hyperactivity and disappearance of spontaneous alternation ('VMT syndrome'). When a specific 6-hydroxy dopamine (6-OHDA) destruction of the dorsal noradrenergic (NA) ascending pathway was superimposed to an electrolytic lesion of the VMT, animals recovered a normal locomotor activity and the possibility to alternate. Since many studies indicate that the development of the 'VMT syndrome' is linked to the disruption of the dopaminergic (DA) meso-cortico-limbic transmission, it is proposed that the recovery observed is due to an interaction between NA and DA ascending systems in cortical and/or subcortical structures; noradrenergic innervation would have a permissive role on the expression of the 'VMT syndrome', possibly via a mechanism of heteroregulation of DA receptors by NA fibers.

Animals↗