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R Bergeron

Publications and source records attributed to R Bergeron.

At least 19 recordsLinked to original sources
PubMed1995

In vivo modulation of sigma receptor sites by calcitonin gene-related peptide in the mouse and rat hippocampal formation: radioligand binding and electrophysiological studies.

Possible interactions between sigma (sigma) receptor sites and calcitonin gene-related peptides (CGRP) were investigated using receptor subtype-related analogues and fragment in in vivo [3H](+)SKF 10 047/sigma binding in the hippocampus, and electrophysiological recording of the N-methyl-D-aspartate (NMDA)-induced activation of CA3 pyramidal neurons, two well-established sigma assays. In both paradigms, CGRP and the agonist [Cys(ACM)2,7]hCGRPalpha modulated sigma systems. In vivo binding experiments demonstrated that CGRP and [Cys(ACM)2,7]hCGRPalpha inhibited 25-40% of specific [3H](+)SKF 10 047 labelling in the mouse hippocampal formation while the purported antagonist hCGRP8-37 was inactive. The specificity of this modulation was demonstrated further by the lack of effect of other vasoactive peptides, including the atrial natriuretic peptide, substance P, and its N-terminal fragment, substance P1-7. In the CA3 subfield of the rat dorsal hippocampus, hCGRP alpha decreased (up to 61%) the NMDA-induced activation of the pyramidal neurons. Conversely, the linear analogue [Cys(ACM)2,7]hCGRP alpha enhanced (by 85%) the NMDA-induced activation of CA3 pyramidal neurons, while the antagonistic fragment hCGRP8-37 had no effect. Haloperidol, a high-affinity sigma receptor ligand, inhibited by 90% the in vivo [3H](+)SKF 10 047 labelling, and prevented the modulation of the NMDA-induced activation by hCGRP alpha and [Cys(ACM)2,7]hCGRP alpha. It thus appears that CGRP can modulate sigma-related systems in the hippocampal formation.

Animals↗
PubMed1995

Biphasic effects of sigma ligands on the neuronal response to N-methyl-D-aspartate.

Previous studies from our laboratory have demonstrated that low doses of selective sigma (sigma) ligands potentiate the neuronal response to N-methyl-D-aspartate (NMDA) in the CA3 region of the rat dorsal hippocampus. Sertraline and clorgyline, two antidepressant drugs with a high affinity for receptors, also potentiate, at low doses, the NMDA response; however, when administered at higher sigma doses, the degree of potentiation induced by these two ligands progressively decreases (Bergeron et al. 1993). In the present experiments, the selective sigma ligands DTG, (+)pentazocine, BD-737, JO-1784 and L-687,384 were studied to determine if they would also generate bell-shaped dose-response curves. These ligands were administered intravenously at doses ranging from 1 micrograms/kg to 1 mg/kg or applied by microiontophoresis. They potentiated selectively, with bell-shaped dose-response curves, the NMDA-induced activation of pyramidal neurons in the CA3 region of the rat dorsal hippocampus. The potentiation of the NMDA response following the intravenous administration of a low dose of a sigma ligand persisted for at least 60 min, after which point in time a second injection of the same dose induced the same degree of potentiation. Moreover, a sustained potentiation was obtained during prolonged microiontophoretic applications of a sigma ligand. These two latter series of observations suggest that the lack of effect of the high doses of sigma ligands is not related to a rapid desensitisation of sigma receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Effect of inhibition of gluconeogenesis on arginine-induced insulin secretion.

It is well known that several amino acids, such as arginine, are potent stimuli for insulin and glucagon secretion from the pancreas. Recently, vagal arginine sensors, which modulate arginine-induced pancreatic hormone secretion, have been reported to exist in the liver. The present investigation was designed to evaluate the role played by gluconeogenesis in this hepatic influence. To this end, we studied the effects of an intraperitoneal injection of 3-mercaptopicolinic acid (3-MPA), a gluconeogenic inhibitor, on the pancreatic hormonal response induced by intraperitoneal administration of arginine (1 g/kg body mass) to hepatic vagotomized and sham vagotomized rats. Fifteen min following the injection of arginine, the increases in glucose and insulin concentrations were significantly lower in rats with an inhibited gluconeogenesis than in rats with an intact capacity for gluconeogenesis. There were no effects of the hepatic vagotomy on the arginine-induced hormonal responses either with or without the 3-MPA injection. The results suggest that gluconeogenesis is implicated in the hepatic modulation of arginine-induced pancreatic hormone secretion.

Animals↗
PubMed1995

The safety of concomitant use of sumatriptan and antidepressant treatments.

It is presently contraindicated to use the antimigraine drug sumatriptan with selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, or lithium. Consequently, many patients undergoing these pharmacotherapies for psychiatric disorders may not benefit from the therapeutic effect of sumatriptan in acute migraine attacks. Because sumatriptan does not appear to cross the blood-brain barrier and has a short half-life, it was deemed relatively safe to prescribe sumatriptan with antidepressant treatments. Fourteen patients receiving fluoxetine, fluvoxamine, sertraline, moclobemide, lithium, or buspirone did not experience significant side effects when they took oral sumatriptan for the relief of migraine on a total of 103 episodes. It is concluded that the combined use of sumatriptan with the above-mentioned antidepressant treatments may be safe.

Administration, Oral↗
PubMed1995

Effectiveness of pindolol with selected antidepressant drugs in the treatment of major depression.

On the basis of a previous report suggesting the effectiveness of the beta-adrenoceptor/5-HT1A antagonist pindolol to accelerate the antidepressant effect of a selective serotonin reuptake inhibitor (SSRI) and to produce a therapeutic effect in drug-resistant depressed patients, these open studies were undertaken to further explore the safety and efficacy of this strategy. In a first study, nine untreated unipolar depressed patients were given the SSRI paroxetine (20 mg/day) together with pindolol (2.5 mg thrice daily). One patient stopped taking pindolol because of increased irritability after 3 days. One week later, seven patients had their Hamilton Rating Scale for Depression Score decreased by more than 50%. In a second study, 19 drug-resistant unipolar depressed patients (9 on paroxetine, 5 on sertraline, 3 on fluoxetine, and 2 on moclobemide) were also given pindolol at the same regimen and were assessed weekly. Two patients (one on sertraline, one on moclobemide) stopped taking pindolol also because of increased irritability after 2 and 3 days, respectively. After 1 week of pindolol addition, 10 patients had a more than 50% decrease of their depression score. By day 14, all of the patients had a score of 10 or less, with the exception of those on sertraline. Improvement was maintained in all patients for at least 28 days on this combination. The results of these studies indicate that pindolol is safe when used in combination with an SSRI or moclobemide. Given the positive results obtained in this second open trial in 28 patients, this treatment strategy should be tested under double-blind conditions to establish its efficacy.

Adult↗
PubMed1995

[Hypercalcemia in cancer patients. Who, when and how to treat?].

The most frequent, potentially fatal, metabolic complication in cancer patients is hypercalcemia. After a discussion of cancer-associated hypercalcemia, we propose an individualized intervention model based on an analysis of the clinical situation, the prognosis, and available treatment options.

Humans↗
PubMed1994

Effect of inhibition of hepatic fatty acid oxidation on metabolic and hormonal responses to exercise in rats.

The purpose of the present study was to assess the effects of 2-mercaptoacetate (MA), an inhibitor of hepatic fatty acid oxidation, on the metabolic and pancreatic hormone response to a prolonged (3 h) swimming exercise. All rats were first adrenodemedullated and were either submitted for 3 weeks to a normal (5% fat) or a medium-fat diet (MF; 18% fat). After being submitted to an exercise swimming habituation programme for one week, rats under both dietary conditions were either injected with a bolus dose of MA (600 mumol/kg; ip) or with a saline solution. MA and saline injected rats were either sacrificed after a 3-h swimming exercise or after a 3-h resting period. Administration of MA was associated with a lower level of beta-hydroxybutyrate after exercise in rats fed the MF diet, higher resting and exercising blood glucose levels in rats fed the MF diet, and higher resting and exercising levels of hepatic glycogen in rats fed a normal diet. There were, however, no significant effects of MA on free fatty acid, insulin, glucagon, epinephrine, and norepinephrine concentrations in both dietary conditions either at rest or after exercise. Therefore, the present data do not provide any evidence that the administration of MA, an inhibitor of hepatic fatty acid oxidation, influences the pancreatic hormonal response to exercise. There was also no evidence of a lowering effect of MA on blood glucose levels during exercise.

3-Hydroxybutyric Acid↗
PubMed1994

The effects of sigma ligands and of neuropeptide Y on N-methyl-D-aspartate-induced neuronal activation of CA3 dorsal hippocampus neurones are differentially affected by pertussin toxin.

1. The in vivo effects of the high affinity sigma ligands 1,3-di(2-tolyl)guanidine (DTG), (+)-N-cyclopropylmethyl-N-methyl-1,4-diphenyl-1- ethyl-but-3-en-1-ylamine hydrochloride (JO-1784), (+)-pentazocine and haloperidol, as well as of those of neuropeptide Y (NPY), on N-methyl-D-aspartate (NMDA)- and quisqualate (Quis)-induced neuronal activations of CA3 pyramidal neurones were assessed, using extracellular unitary recording, in control rats and in rats pretreated with a local injection of pertussis toxin (PTX), to evaluate the possible involvement of Gi/o proteins in mediating the potentiation of the neuronal response to NMDA by the activation of sigma receptors in the dorsal hippocampus. 2. Microiontophoretic applications as well as intravenous injections of (+)-pentazocine potentiated selectively the NMDA response in control rats as well as in PTX-pretreated animals. In contrast, the PTX pretreatment abolished the potentiation of the NMDA response by DTG, JO-1784 and NPY. Moreover, microiontophoretic applications of DTG induced a reduction of NMDA-induced neuronal activation. Neither in control nor in PTX-treated rats, did the sigma ligands and NPY have any effect on Quis-induced neuronal response. 3. In PTX-treated rats, the potentiation of the NMDA response induced by (+)-pentazocine was suppressed by haloperidol, whereas the reduction of the NMDA response by DTG was not affected by haloperidol. 4. This study provides the first in vivo functional evidence that sigma ligands and NPY modulate the NMDA response by acting on distinct receptors, differentiated by their PTX sensitivity.

Animals↗
PubMed1994

Effect of hepatic portal infusion of pyruvate on pancreatic hormone response during exercise.

The purpose of the present investigation was to evaluate the effects of a small infusion of pyruvate into the hepatic portal vein on the pancreatic hormone response during exercise (30-min treadmill run; 26 m/min, 0% grade) in adrenodemedullated rats. Resting and exercising rats were infused with either pyruvate (5% solution; 0.016 ml/min) into the portal vein, pyruvate into the jugular vein, or saline into the portal vein. Peripheral and portal blood glucose concentrations were decreased (P < 0.01) similarly in all groups after the exercise period. Peripheral insulin, glucagon, and norepinephrine levels, either at rest or after exercise, were not significantly affected by the infusions. The response of portal pancreatic hormone concentrations to exercise was, however, reduced by the pyruvate infused into the portal and jugular veins for insulin and into the portal vein only for glucagon. The normal increase in peripheral glucagon-insulin molar ratio during exercise was shut down by the infusion of pyruvate into the portal vein but not by the infusion of pyruvate into the jugular vein or by the infusion of saline. These results indicate that a small blood infusion of pyruvate, even in the presence of a decreasing blood glucose level, can attenuate substantially the pancreatic hormone response during exercise in adrenodemedullated rats.

Animals↗
PubMed1993

A comparison of the iron-clearing properties of parabactin and desferrioxamine.

A comparative study of the iron-clearing properties of subcutaneously administered desferrioxamine and parabactin is presented. The evaluation was performed in both a non-iron-overloaded bile-duct cannulated rat and an iron-loaded Cebus monkey model. Parabactin was superior to desferrioxamine in both the rodent and the primate. Unlike desferrioxamine, nearly all of the parabactin-induced iron clearance occurred in the bile. This study represents an evaluation of the iron-clearing properties of parabactin, a hexacoordinate catecholamide siderophore.

Animals↗
PubMed1993

Modification of the N-methyl-D-aspartate response by antidepressant sigma receptor ligands.

Sertraline, a selective serotonin reuptake inhibitor, and clorgyline, a monoamine oxidase inhibitor, both of which have high affinity for sigma receptors, were assessed in an electrophysiological model. In keeping with previous data obtained with other sigma receptor ligands, low doses of sertraline and of clorgyline potentiated selectively with a bell-shaped dose-response curve the effect of N-methyl-D-aspartate (NMDA) on pyramidal neurons in the CA3 region of the rat dorsal hippocampus. This potentiation was reversed by the sigma receptor ligands haloperidol and BMY-14802. The selective serotonin reuptake inhibitor paroxetine and the monoamine oxidase inhibitor tranylcypromine, both devoid of affinity for sigma receptors, had no effects on the NMDA response. These data suggest that the effects of sertraline and clorgyline on the NMDA response are due to their affinity for sigma receptors.

1-Naphthylamine↗
PubMed1992

Determinants of thymotropism in Kaplan radiation leukemia virus and nucleotide sequence of its envelope region.

Radiation leukemia viruses (RadLVs) are a group of murine leukemia viruses which are induced by radiation and cause T-cell leukemia. Viral clones isolated from the BL/VL3 lymphoid cell line derived from a thymoma show variable tropism and leukemogenic potential. We have constructed chimeric viruses by in vitro recombination between two viruses, a RadLV that is thymotropic and an endogenous ecotropic virus that is nonthymotropic. We show here that, in contrast to thymotropism determinants identified previously, which lie in the long terminal repeat (LTR), it is the envelope region that is responsible for the thymotropism of BL/VL3 RadLV. The nonthymotropic virus which we have rendered thymotropic by transfer of the env region of RadLV in the present study has been shown previously to become thymotropic when the LTR of another thymotropic virus is inserted in its genome. Thus, the LTR and envelope gene may be involved in complementary action to lead to thymotropism.

Amino Acid Sequence↗
PubMed1989

Combination iron depletion therapy.

Iron (Fe) depletion with anti-transferrin (Tf) receptor monoclonal antibodies (MAbs), Fe chelators, or gallium (Ga) salts inhibits in vitro and in vivo growth of tumor cells. The present studies examined the cytotoxic effects of an IgA anti-human Tf receptor MAb, 42/6, combined with parabactin, a powerful Fe chelator, or Ga nitrate. Parabactin inhibited in vitro growth of human hematopoietic and solid tumor cells, and the rank order of their sensitivities to the Fe chelator was identical to their relative sensitivity to MAb 42/6 as demonstrated in previous studies. When the most parabactin and MAb 42/6-sensitive (HL60 leukemia) and -resistant (KB carcinoma) cells were incubated with various concentrations of parabactin, cell killing was time and dose dependent over the first 24 hours. Little additional cytotoxicity occurred, however, when cells were exposed to parabactin for 48 hours. HL60 cells were slightly more sensitive than KB cells to parabactin cytotoxicity. Addition of optimally effective concentrations of anti-Tf receptor MAb 42/6 to parabactin increased cytotoxicity to HL60 cells over a narrow parabactin dose range but had little effect on cytotoxicity to KB cells. Cell cycle analysis of cells treated with parabactin for 24 hours showed that doses causing variable cytotoxicity increased the percentage of cells in S phase, but higher parabactin concentrations consistently arrested cells in G1 phase or at the G1/S interface. MAb 42/6 also increased toxicity of parabactin to granulocyte/macrophage colony-stimulating factors and normal marrow granulocyte/macrophage progenitors. When HL60 or KB cells were treated with MAb 42/6 combined with Ga nitrate, MAb 42/6 increased cytotoxicity of Ga for HL60 cells but had little or no effect on Ga cytotoxicity to KB cells. In contrast, MAb 42/6 had minimal effects on cytotoxicity of the ribonucleotide reductase inhibitor, isoquinaldehyde thiosemicarbazone, to either HL60 or KB cells. Both hematopoietic and solid tumors were killed by Fe depletion, but the present studies suggested that hematopoietic cells are more sensitive than solid tumor cells to cytotoxic effects of Fe depletion. Combined Fe depletion therapy by the use of MAb 42/6 with an Fe chelator or Ga salt increased toxicity to MAb 42/6-sensitive cells, such as HL60, but was not more effective against MAb 42/6-resistant solid tumor cells. Combination Fe depletion therapy of hematopoietic cell tumors merits evaluation in experimental in vivo tumor systems.

Antibodies, Monoclonal↗
PubMed1985

Relative brain size and metabolism in birds.

Earlier studies have shown that the negatively allometric brain-body weight association in mature mammals changes to an isometric association when body weights are adjusted for their rates of oxygen consumption. Birds are endogenous homeotherms, and so their brain weights were analyzed according to their body weights and metabolism (estimated energy supply). As expected, the brain and body weights of the 83 species of neognathid birds have a negatively allometric association. The same species, however, have a brain weight-to-estimated energy supply which cannot be separated from isometry. While passerines have bigger brains for their body weights than altricial nonpasserines, the relative brain sizes of the two avian groups cannot be separated once the metabolic rate is used to adjust the body weights. Ratites or paleognathid birds may have a different brain-to-metabolism association. Consideration of bioenergetics helps clarify brain and body weight associations.

Animals↗
PubMed1975

Complex formation between mycobacterial polysaccharides or cyclodextrins and palmitoyl coenzyme A.

The mycobacterial polysaccharides MMP (3-O-methyl-mannose-containing polysaccharide), MGLP (lipolysaccharide containing 6-O-methylglucose and glucose), and the cyclodextrins (cyclohexaamylose and cycloheptaamylose) form stoichiometric complexes with palmitoyl-CoA (Machida, Y., Bergeron, R., Flick, P., and Bloch, K. (1973) J. Biol. Chem. 248, 6246-6247). Complex formation is presumed to result from hydrophobic interactions. In order to enhance the hydrophobic character of the cyclodextrins the following derivatives have been synthesized: heptakis (2,di-O-propyl)-, heptakis (2,6-di-O-methyl)-, pentakis (6-O-methyl)-, heptakis (3-O-methyl)-, and permethylated beta-cyclo-dextrin. These compounds stimulate fatty acid synthesis catalyzed by the Mycobacterium smegmatis fatty acid synthetase, the magnitude of the effect decreasing in the order in which the alkylated cyclodextrins are listed above. MMP or MGLP are qualitatively indistinguishable from alkylated cyclodextrins both with respect to palmitoyl-CoA binding and with respect to effects on enzyme systems, suggesting that they form inclusion complexes of the same type. On the basis of model building it is postulated that MMP in solution assumes a helical conformation with a hydrophobic channel about 6 A in diameter and approximately 29 A long, dimensions appropriate for accommodating the paraffinic chain of palmitoyl-CoA in the form of an inclusion complex. Since palmitoyl-CoA binds to polysaccharide much more tightly than free palmitate it is further postulated that ionized groups of the CoA moiety of acyl CoA participate in the binding and do so by hydrogen bonding to the hydrophilic exterior of helical MMP. Palmitoyl-CoA, and to a lesser extent palmitate, affect the optical rotation of MMP and also of the alkylated cyclodextrins indicating that complex formation induces conformational changes in the polysaccharides.

Binding Sites↗