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F Lebrun

Publications and source records attributed to F Lebrun.

At least 37 records · Page 2Linked to original sources
PubMed1996

Exposure to either gamma or a mixed neutron/gamma field irradiation modifies vasoactive intestinal peptide receptor characteristics in membranes isolated from pig jejunum.

The effect of acute whole body exposure to ionizing radiation was investigated on intestinal vasoactive intestinal peptide (VIP) receptors and adenylate cyclase activity in membranes isolated from pig jejunum. Pigs under light anaesthesia were exposed to a single dose (6 Gy) of gamma (gamma) or to mixed neutron/gamma field (ratio 1:1; neutron/gamma) irradiation. Seven days after irradiation, plasma-membranes were prepared from post mortem jejunal mucosal scrapings. Marker enzyme activities (sucrase, leucine aminopeptidase (LAP), Na,K-ATPase) were measured in each preparation. The characteristics (KD, Bmax) of VIP receptors were determined using 125I-labelled VIP. In addition VIP-sensitive adenylate cyclase activity was measured. Results showed that enzyme activities were reduced following both gamma (sucrase 67%; LAP 53%; Na/K-ATPase 29%; N = 7) and neutron/gamma (sucrase 53%; LAP 59%; Na/K-ATPase 68%; N = 5) compared with control values (N = 5). VIP receptor affinity was decreased following either type of irradiation (gamma or neutron/gamma P < 0.01) and receptor numbers increased. Both VIP- and forskolin-stimulated adenylate cyclase activities were reduced but the sensitivity of the enzyme remained the same for VIP (EC50 values (nmol dm-3)-control-1.27 +/- 0.35; gamma-2.18 +/- 0.41; neutron/gamma-1.91 +/- 0.28). In conclusion, exposure to either gamma or neutron/gamma irradiation attenuates intestinal enzyme activities and VIP receptor affinity but increases VIP receptor numbers.

Adenylyl Cyclases↗
PubMed1995

The parietal sheet of Bowman's capsule of rat renal glomerulus: a target of endothelin and PAF.

On the basis of intracellular calcium concentration ([Ca2+]i) measurements, we have previously reported that the parietal sheet of Bowman's capsule was sensitive to cholinergic agonists. The aim of the present work was to investigate whether this structure could be also a target of endothelin and platelet-activating factor (PAF), since we observed [Ca2+]i increases in response to both agonists in the glomerulus, but which were very different from that induced by carbachol. For this purpose, we measured [Ca2+]i on single microdissected parietal sheets, using a fura 2 microfluorescence technique and compared the effects of maximal concentrations of the three agonists (10(-7), 10(-8), and 10(-4) M for endothelin, PAF, and carbachol, respectively) under various experimental conditions. We observed that, like in the glomerulus, endothelin and PAF induced, in the parietal sheet, [Ca2+]i responses that differed in many respects from those found with carbachol. Thus, in the presence of 2 mM external calcium, 1) endothelin and PAF responses spontaneously declined to basal level, whereas a stationary plateau was observed after a sharp peak of [Ca2+]i with carbachol; 2) the magnitude of [Ca2+]i peak was smaller with endothelin and PAF than with carbachol; and 3) endothelin and PAF, but not carbachol, induced a homologous dose-dependent desensitization. Moreover, in the absence of external calcium, endothelin and PAF responses were smaller than carbachol response, although all three responses apparently resulted from release of calcium ions from the same internal pool. In additional experiments, we observed that, like carbachol, endothelin and PAF contracted the parietal sheet, which is only composed of myoepithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Kainate-induced status epilepticus leads to a delayed increase in various specific glutamate metabotropic receptor responses in the hippocampus.

Neuronal loss and gliosis were detected in the rat hippocampus soon after unilateral intra-amygdala injection of kainate (KA) (2.5 nmol) while solid mossy fiber sprouting could be seen only fourteen days after this injection. Using this experimental model, we examined the metabotropic glutamate receptor (mGluR)-induced inositol phosphate (IP) formation in hippocampal synaptoneurosomes and slices. In synaptoneurosomes prepared from ipsilateral hippocampi fourteen days following injection, there were no significant changes in mGluR- and carbachol(CARB)-stimulated IPs syntheses when sham-operated and KA-injected animals were compared. In the corresponding hippocampal slices, significant increases of the mGluR responses mediated by ibotenate (IBO) and aminocyclopentane-trans-1,3-dicarboxylate (t-ACPD) were noted after KA application. The net stimulation values respectively expressed in a pair-wise fashion for buffer-injected control and KA-treated animals were IBO: 1,947 +/- 457 and 10,553 +/- 1,242; t-ACPD: 1,557 +/- 662 and 9,449 +/- 2,251 dpm/mg protein respectively. Significantly augmented mGluR responses in hippocampal slices were also measured at 7, 42 and 92 days after KA injection. There were, however, no significant increases in CARB-stimulated phosphoinositide hydrolysis in the hippocampal slices at all time-intervals after KA administration. These findings show that there are differences between the mGluR responses in hippocampal synaptoneurosome and slice preparations, suggesting the presence of two distinct populations of mGluR in each of these two models. The large specific increases in certain mGluR activities after KA-induced status epilepticus in hippocampal slices could represent one of the molecular mechanisms which underlie the profound morphological changes, in particular gliosis or mossy fiber sprouting, which follow the KA-induced status epilepticus.

Animals↗
PubMed1994

Ontogenesis of quisqualate-associated phosphoinositide metabolism in various regions of the rat nervous system.

The effect of postnatal age on phosphoinositide metabolism per se and on quisqualate-stimulated phosphoinositide metabolism was characterized in synaptoneurosomes prepared from nine different regions of the rat nervous system, namely the brainstem, cerebellum, cerebral cortex, colliculi, hippocampus, hypothalamus, olfactory bulb, spinal cord and striatum. In the hippocampus, striatum, cerebellum, cerebral cortex, brainstem, colliculus and spinal cord, the basal levels of inositol phosphate (inositol-1-phosphate+inositol-4,5-bisphosphate) formation were maximal two days after birth and declined steeply to steady-state levels from the age of 10 postnatal days. Similarly, in the olfactory bulb, basal inositol phosphate synthesis did not significantly change when measured during the period from postnatal day 10 to 42. The extent of [3H]-inositol labelling of phosphoinositides as a function of age presented similar profiles when measured in hippocampal, striatal, cerebellar and cerebral cortical synaptoneurosomes, i.e. maximal at perinatal ages and minimal at adult ages. In the hypothalamus, [3H]-inositol labelling of phosphoinositides showed an increase from postnatal day 12 to higher levels from postnatal days 14 to 18 subsequently followed by a dramatic increase from postnatal day 21 to 42. A similar developmental trend was also obtained for basal inositol phosphate synthesis. On the whole, four types of developmental profiles for quisqualate-stimulated inositol phosphate formation (expressed as the percentage of the basal level and as the difference between stimulated and basal levels of radioactive inositol phosphates) were obtained depending on the nervous system region studied. In the early, prenatally developed nervous system regions, namely the brainstem and the spinal cord, no postnatal stimulation peaks of quisqualate-induced inositol phosphate formation were recorded. This was also the case for the colliculi when the stimulation of IP formation was expressed as the difference in basal and stimulated levels of inositol phosphates. Secondly, in the olfactory bulb a region known to possess a continuous capacity for developmental plasticity both structurally and functionally during the first three weeks of postnatal development, a simultaneous sustained high level of quisqualate stimulation of phosphoinositide metabolism (fluctuating around 200% of the basal level) during the early postnatal period was evident. Thirdly, in regions of the central nervous system like the cerebellum, cerebral cortex, hippocampus and the striatum known to undergo intense developmental activity during the first two postnatal weeks, peaks of quisqualate-stimulated phosphoinositide metabolism were initially detected around the first week after birth in each of these brain areas.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

A study of GABAergic system in Scrapie-infected hamsters after striatal microinoculation of the agent.

Experimental Scrapie in hamster is a simple, reproducible model of prion diseases that occur in humans and animals. Stereotaxic microinoculation (0.5 microliter) of the agent (263 K) into a specific cerebral structure (striatum) in hamster, previously developed in our group, gives the opportunity to further investigate the pathogenesis of these degenerative diseases and to more precisely define the brain areas and the groups of cells more vulnerable to the effects of the agent. In this model, early significant changes of glutamic acid decarboxylase (GAD) activity in striatum suggested a preferential alteration of the GABA system. The present study was focused on the effects of Scrapie agent directly injected into striatum on GABA neurons at the presynaptic level (GABA uptake) and at the postsynaptic level (GABAA receptors). The high-affinity [3H]GABA uptake is not changed in the Scrapie-injected striatum neither in the controlateral site and the kinetics (Km, Vmax) values are not statistically different for control and Scrapie-inoculated animals. The binding of [3H]GABA (Scatchard analysis) to cerebral membranes does not seem to be altered either at the local site of agent inoculation (striatum) neither at distance in the cerebellum: the affinity constant (Kd) to the ligand and the maximal number of receptor sites were of the same magnitude in control and Scrapie animals, but we do not have a statistical analysis. These effects are completely different of those of a neurotoxin. The present data suggest that the effects of prion agent may be very limited and very specific to some cellular mechanisms, without altering the whole cellular machinery, as recently shown in an in vitro model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Functional dyspepsia versus other functional gastrointestinal disorders: a practical approach in Belgian general practices.

This paper identifies the symptom profile associated with the four main diagnoses of functional digestive disorders (dyspepsia, gastro-oesophageal reflux disease (GORD), gastritis, and constipation) made by general practitioners in Belgium. Results are also presented from a multicentre study in which the effects of cisapride, administered as an oral tablet or suspension, were evaluated in patients with these functional digestive disorders. Analysis of symptom patterns revealed that early satiety and postprandial abdominal bloating were the most prominent symptoms, followed by eructation (belching), heartburn, regurgitation, postprandial epigastric burning or discomfort, and nausea. These symptoms occurred in all diagnostic groups. However, different symptom patterns were associated with each of the disorders; for example, heartburn and regurgitation were the core symptoms in patients diagnosed as having GORD, early satiety and abdominal bloating were characteristic of patients diagnosed with dyspepsia, and fasting or postprandial pain were characteristic of patients given the diagnosis of gastritis. Therefore, it appears that these diagnoses used by general practitioners in Belgium closely correspond to reflux-like, dysmotility-like and ulcer-like dyspepsia, as defined by an international working party. Cisapride improved the core symptoms in about 80% of patients with GORD or dyspepsia, relieved all epigastric symptoms in about 80% of patients with gastritis, and significantly decreased the use of laxatives and increased stool frequency in constipated patients. Cisapride was well tolerated and thus appears to be a useful option in the treatment of functional digestive disorders in a general practice setting.

Adult↗
PubMed1992

Cholinergic effects on intracellular free calcium concentration in renal corpuscle: role of parietal sheet.

To investigate a possible effect of cholinergic agonists on the renal glomerular function, fura-2 microfluorometric measurements of intracellular free calcium [( Ca2+]i) were performed on single intact glomeruli, single isolated parietal sheets of the Bowman's capsule and single parietal sheet-deprived glomeruli (PS-D glomerulus). Carbachol (10(-4) M), in the presence of 2 mM external calcium, induced a biphasic increase in [Ca2+]i characterized by a sharp initial peak followed by a sustained plateau in the whole glomerulus (delta [Ca2+]i = 177 +/- 13 and 70 +/- 7 nM, respectively; n = 21) and in the parietal sheet (418 +/- 30 and 111 +/- 13 nM, respectively; n = 21). In the PS-D glomerulus (n = 9), the response was less marked and included a barely visible peak (77 +/- 13 nM) and a relatively low plateau (49 +/- 11 nM). In the absence of external calcium, the peak phase was preserved in the three structures, indicating a calcium release from intracellular pools, whereas the plateau, due to the entry of external calcium, was suppressed. These effects were fully inhibited by 10(-4) M of either atropine or pirenzepine, demonstrating the muscarinic nature of the receptors. Dose-response curves showed that the parietal sheet was more sensitive to the physiological agonist (acetylcholine) than to carbachol. A still unexplained difference in sensitivity was noted between peak and plateau, respectively (half-maximal responses were 5 x 10(-6) vs. 5 x 10(-7) M for carbachol and 2 x 10(-7) vs. 3 x 10(-8) M for acetylcholine).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

A specific transduction mechanism for the glutamate action on phosphoinositide metabolism via the quisqualate metabotropic receptor in rat brain synaptoneurosomes: I. External Na+ requirement.

The characteristics of the transduction mechanism(s) activated by glutamate (Glu) via the quisqualate metabotropic receptor, as well as by depolarizing agents, to trigger formation of inositol phosphates (IPs) were investigated in 8-day-old rat forebrain synaptoneurosomes. The replacement of external Na+ by various compounds (Li+, Tris+, N-methyl-D-glucamine+, and sucrose) induces an increase in basal accumulation of IPs and depolarizes synaptoneurosome membranes. Under these conditions, Glu- and K(+)-induced accumulations of IPs are inhibited, whereas the carbachol (Carb)-elicited response of IPs parallels the basal one. Agents increasing Na+ influx, such as veratridine and monensin, depolarize synaptoneurosomes and stimulate formation of IPs. These stimulations are not additive with responses of IPs elicited by Glu or K+. These data suggest that (a) Glu activates phosphoinositide metabolism via a specific mechanism (distinct from that of cholinergic agonists), (b) depolarizing agents and Glu share at least one common intermediate step in their mechanisms of activation of the metabolism of IPs, and (c) the depolarization may correspond to this common step. In addition, Na+ seems to be required for Glu stimulation of metabolism of IPs. The depolarization associated with the action of Glu on formation of IPs results neither from an influx via tetrodotoxin-sensitive voltage-dependent Na+ channels nor from an entry via the classically characterized Na+/Ca2+ or Na+/H+ exchangers. In fact, tetrodotoxin (2 microM) has no effect on the Glu- or K(+)-elicited response of IPs. Amiloride (greater than 50 microM) and some of its derivatives similarly inhibit not only Glu- and K(+)- but also Carb-evoked formation of IPs.

Amiloride↗
PubMed1990

Cholinergic agonists increase cell calcium in rat medullary collecting tubules. A fura-2 study.

The intracellular free calcium concentration [Ca2+]i of rat medullary collecting tubules was calculated from microscope fluorescence measurements in single pieces of fura-2-loaded tubules superfused at 37 degrees C. When carbachol (10(-4)-10(-3) M) was added in the superfusate, a biphasic increase in [Ca2+]i was generally obtained, which included an early peak phase and a sustained plateau thereafter; sometimes, the peak phase was not apparent; the plateau was maintained as long as the agonist was applied. Several responses could be induced successively without a fall in responsiveness. From dose/response curves, K1/2 values of about 10(-5) M for carbachol and 10(-6) M for acetylcholine were obtained. The effects of the agonists were suppressed with 10(-4) M of atropine or pirenzepine, indicating the presence of muscarinic receptors of the M1 type. In the absence of external calcium, the peak phase of the response was preserved while the plateau phase was suppressed; thus, the peak involves the release of calcium stored in organelles, whereas the plateau involves the entry of external calcium through calcium channels which were voltage independent and insensitive to the usual calcium blockers.

Acetylcholine↗
PubMed1988

[Not Available].

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France↗
PubMed1985

[Safety of term birth and cesarean birth rates].

This was a parallel of the rate of caesarean section and neurological morbidity of the term newborn. This study was performed on all infants born at a gestational age of 37 weeks or greater in 1981 and 1982 at the Baudelocque Maternity Hospital. The results show a stable caesarean section rate during these two years: 21% in 1981, 20% in 1982; as for the safety of term birth there was only one case of perinatal insult during a vaginal birth responsible for cerebral dysfunction of moderate degree. There was a 18% operative maternal morbidity and there were no deaths. We concluded that a caesarean section rate of 20% in a University Hospital is justified by the virtual absence of neonatal morbidity with an acceptable maternal risk. This rate should not increase. The possible ways of decreasing this rate, while maintaining neonatal safety, must be studied. The original aspect of this work concerns the monitoring of the caesarean section rate by the incidence of neurological complications of all term births during a fixed period of time.

Cesarean Section↗
PubMed1984

Respiratory pauses in very low risk prematurely born infants reaching normal term. A comparison to full-term newborns.

We studied the occurrence of greater than or equal to 2 sec. respiratory pauses (RP) in very low risk, normal prematurely born infants (less than or equal to 36 wks. of gestation), recorded when they reached 37-40 wks. conceptional age and compared the results with those of full-term (37-41 wks. of gestation) newborns. The influence of gestational age at birth (GA), postnatal age, sleep states, twin birth and gross body movements was tested. We recorded 2434 central RP and only one 4 sec. duration obstructive RP. We never observed RP greater than 15 sec. 10-15 sec. RP were rare, noted only in 37-38 wks. GA newborns. We found some differences between prematures reaching normal term on one hand and full-term newborns on the other: a) RP frequency and periodic breathing were higher in prematurely born infants; b) Between-sleep state differences leveled out in prematures reaching normal term (they had more numerous RP in all sleep states), while the prevalence of RP in active sleep compared to quiet sleep was constant in full-term newborns. There were no significant differences between prematurely born twins and singletons. When they reached normal term, infants born before 35 wks. of gestation had more RP, compared to infants born at 35-36 wks. of gestation. About 12% of RP occurred after gross body movements.

Diseases in Twins↗