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S Trottier

Publications and source records attributed to S Trottier.

At least 37 records · Page 2Linked to original sources

Cerebral distribution of the B-36 VDAC protein in rat, cow and man brain: immunocytochemical study.

Polyclonal antiserum to a new voltage-dependent anion channel protein (B-36 VDAC) isolated during the purification of the GABAA receptor from bovine cerebral cortex was used to determine the localization of this protein in immunocytochemical preparations of cerebral cortex, cerebellum and hippocampal formation of rat, cow and human. The labeling was present in the Purkinje cells and some cells of the molecular layer of the rat cerebellum, as well as in pyramidal and non-pyramidal cells of the rat and human cerebral cortex; the labeling outlined the membrane surface. In the rat granule cells of the dentate gyrus and the pyramidal cells, the labelling was observed within the cells. These results indicate that the B-36 VDAC protein is heterogeneously distributed among different cerebral regions in different species and suggest that this protein would be associated with the alpha-1 subunit of the GABAA receptor (benzodiazepine binding sites).

Animals↗

Polyamine metabolism in epileptic cortex.

Polyamine (tissue) concentrations have been studied in hippocampus and temporal neocortex from patients with temporal lobe epilepsy. Depth electrode recordings demonstrated hippocampal origin of the seizures, the temporal neocortex being involved during the discharge propagation. Neuropathological examination of excised tissues showed glial proliferation or glioma in Ammon's horn (CA), whereas the temporal neocortex did not exhibit any histological abnormality. Polyamine (putrescine or PUT, spermidine or SPD, spermine or SPM) concentrations were determined on surgical samples from the hippocampus and various areas of temporal neocortex. Human post-mortem tissue from temporal lobe regions was used for controls. In post-mortem controls and temporal neocortex specimens from epileptic patients, polyamine levels were similar (in nmol/g wet weight: PUT = 40-100; SPD = 200-350; SPM = 100-200). In CA, polyamine levels exhibited striking changes: SPD content was significantly increased (350-700 nmol/g) while SPM was lowered (50-100). PUT was only increased in CA invaded by the tumoral process (100-180). Accordingly, a very high SPD/SPM molar ratio in the abnormal CA region was observed, indicating an acceleration of polyamine neosynthesis which is usually related to ornithine decarboxylase induction. Metabolic changes in polyamines appear to be selective of human epileptic hippocampus. A relationship between glial proliferation (gliosis or neoplasia), epileptic firing and polyamines is discussed.

Adult↗

Surgical therapy for frontal epilepsies.

We have described our 25 years experience concerning 100 patients operated on for frontal epilepsy. Results show that 55% of patients are practically cured of their seizures and that 76% benefited from cortectomy (reduction of more than 75% of seizures). These results are the worst in the total series of St. Anne. Reasons for success and especially failure were analyzed in detail: 1. SEEG methods gave good indications along three dimensions of the limits and borders of the cortical excision. 2. When clinical semiology and organization of ictal discharges give evidence for rapid bilateral discharge, with involvement of axial musculature and generalized tonic-clonic manifestations, experience shows that it is necessary to combine cortectomy with a section of the adjacent cortico-subcortical fibers of the corona radiata, as if propagation of ictal discharges were impeded if not interrupted by sectioning such fibers and the primary site were incapable of expressing itself clinically. 3. If the characteristics of seizures suggest the quasisimultaneous involvement of the two frontal lobes and the existence of bilateral multifocal epilepsy, we suggest that a systematized anterior callosotomy might lead to useful results. 4. Finally, we propose general criteria for indications and contraindications for surgery.

Adolescent↗

Haemophilus influenzae causing conjunctivitis in day-care children.

The role of Haemophilus influenzae in acute purulent conjunctivitis was studied during an outbreak among children in day care. Five day-care centers contributed 20 cases and 35 controls. All the children were subjected to culture of the nasopharynx and the eyes. H. influenzae was carried in the nasopharynx of 53% of the children (range between day care centers, 20 to 91%). Of the 20 children with acute conjunctivitis 8 had eye cultures positive for H. influenzae, 2 had Moraxella and the remaining were culture-negative. Ten colonies of H. influenzae were isolated from each positive culture and identified by capsular type, biotype and multi-locus enzyme electrophoresis. All but one of the isolates were nonencapsulated. They belonged to 4 biotypes and 8 electrophoretic types. The same strain was recovered from the eyes and nasopharynx of the symptomatic children, suggesting that the H. influenzae in the eyes originated from the nasopharynx. There was no evidence for spread of the same H. influenzae strains between day-care centers. Even within each center the Haemophilus strains recovered from the eyes varied among the symptomatic children. The in vitro capacity to attach to oropharyngeal epithelial cells was not increased among the H. influenzae recovered from the eyes. The results question if the majority of conjunctivitis cases were caused by H. influenzae and suggested that eyes were colonized with the nasopharyngeal carrier strain rather than infected by an isolate with special virulence for the eye.

Bacterial Adhesion↗

Concentrations of teicoplanin in serum and atrial appendages of patients undergoing cardiac surgery.

The concentrations of teicoplanin in sera and heart tissues of 49 patients undergoing coronary bypass were measured. Each patient received a 6- or 12-mg/kg dose of teicoplanin administered in a slow intravenous bolus injection over 3 to 5 min beginning at the time of induction of anesthesia. Mean +/- standard error of the mean concentrations in serum were, for the two doses, respectively, 58.1 +/- 1.7 and 123.3 +/- 7.4 micrograms/ml 5 min after administration and 22.2 +/- 0.7 and 56.5 +/- 2.8 micrograms/ml at the time of removal of atrial appendages. Mean +/- standard error of the mean concentrations in tissue were 70.6 +/- 1.7 and 139.8 +/- 2.2 micrograms/g, respectively, giving mean tissue/serum ratios of 3.7 +/- 0.3 and 2.8 +/- 0.2, respectively. Teicoplanin penetrates heart tissue readily and reaches levels in the serum far in excess of the MICs for most pathogens that have been found to cause infections following open heart surgery.

Anti-Bacterial Agents↗

Co-localization of tyrosine hydroxylase and GABA immunoreactivities in human cortical neurons.

Samples of human cerebral cortex were stained immunocytochemically for tyrosine hydroxylase (TH) and gamma-aminobutyric acid (GABA). TH-positive neurons were in small number and predominated in the deep infragranular layers V-VI contrasting with numerous GABA-positive neurons scattered in all layers. Co-localization of TH- and GABA-like immunoreactivities in a single cell was studied by the double immunolabeling technique with the elution-restaining procedure. Only 50% of the TH-positive neurons also expressed GABA-like immunoreactivities. The two markers were detectable in the somata and not in the processes of the cells. The double-labeled cells were mainly fusiform and medium-sized and were observed in layer VI. These observations suggest that the TH-positive cells form a mixed neuronal population, only a part of which corresponds to the GABAergic class of intrinsic interneurons.

Cerebral Cortex↗

Changes in GABA-immunoreactive cell density during motor focal epilepsy induced by cobalt in the rat.

The distribution of GABA-immunoreactive cell bodies and terminals was studied using an anti-GABA serum during the development of chronic focal epilepsy induced by cobalt deposits onto the motor cortex of the rat. Cell counts of GABA-positive neurons were carried out in the epileptogenic area and correlated with the electrophysiological activity of the cobalt focus. In normal control rats, we identified GABA-immunoreactive somata and processes in the motor agranular cortex; they were multipolar or bipolar but never pyramidal and were present in all layers, especially in layer II. GABA-immunoreactive terminals were widely scattered in the neuropil and surrounded the unlabelled cell bodies. In the cobalt-treated animals, changes in the GABAergic innervation were observed during the development of the epileptic focus: decreases in the GABA-positive cell density and in the number of GABA-positive terminals were present before the onset of epileptic discharges and became more marked during the period of maximal spiking activity; a progressive return to normal values of GABA-positive cell density (except in the deep layers) as well as the reappearance of GABA positive terminals were associated with the extinction of the epileptic syndrome. Our observations suggest that the impaired inhibitory neurotransmission mediated by GABA plays a role in the development of the cobalt-induced epilepsy; moreover the recovery of GABAergic function which occurs during the extinction of the epileptic syndrome might imply a capacity for axonal regeneration of the GABAergic neurons.

Animals↗

Turnover of nontypable Haemophilus influenzae in the nasopharynges of healthy children.

The nasopharyngeal Haemophilus influenzae flora of healthy children in a day care center was analyzed by repeated sampling during 4 winter months. The average carrier rate was 39%, but 74% of the children became colonized at some time during the study. The H. influenzae isolates were identified by capsular type, biotype, and multilocus enzyme electrophoresis. The turnover of the flora in individual children and in the day-care group was characterized. Four patterns of colonization were defined among the 38 children and 49 H. influenzae strains. Depending on the persistence in the group, the strains were designated as endemic, i.e., shared between several children on several occasions, or as epidemic, i.e., occurring only once but in several children. The individual hosts had two patterns; resident strains persisted for 2 weeks or more, and transient strains showed no evidence of persistence. The results suggest that there is considerable sharing of certain nontypable H. influenzae among healthy children in day care, whereas other strains remain restricted to a single host. The properties of host and bacteria determining these patterns remain to be defined.

Child↗

Regional and laminar distribution of the dopamine and serotonin innervation in the macaque cerebral cortex: a radioautographic study.

The regional density and laminar distribution of dopamine (DA) and serotonin (5-HT) afferents were investigated in the cerebral cortex of cynomolgus monkeys using a radioautographic technique that is based on the high affinity uptake capacity of these aminergic neurons. Large vibratome sections, 50 micron thick, were incubated with [3H] DA (0.2 microM) and desipramine (5 microM) or with unlabeled norepinephrine (5 microM) and [3H] 5-HT (0.6 microM), which allowed for the specific labeling of the DA and 5-HT innervations, respectively. After fixation, these sections were dried, defatted, and radioautographed by dipping. Semiquantitative data on the DA innervation also were provided by counting [3H] DA-labeled axonal varicosities in radioautographs from 4-micron-thick sections of the slices obtained after epon embedding. The DA innervation was widespread and differed in density and laminar distribution in the agranular and granular cortices. DA afferents were densest in the anterior cingulate (area 24) and the motor areas (areas 4, 6, and supplementary motor area [SMA]). In the latter they displayed a trilaminar pattern of distribution, predominating in layers I, IIIa, and V-VI, with characteristic cluster-like formations in layer IIIa, especially in the medial part of motor areas. In the granular prefrontal (areas 46, 9, 10, 11, 12), parietal (areas 1, 2, 3, 5, 7), temporal (areas 21, 22), and posterior cingulate (area 23) cortices, DA afferents were less dense and showed a bilaminar pattern of distribution, predominating in the depth of layer I and in layers V-VI; density in layers II, III, and IV was only 20% of that in layer I. The lowest density was in the visual cortex, particularly in area 17, where the DA afferents were almost restricted to layer I. The density of 5-HT innervation was generally greater than that of DA except in the motor areas and in the anterior cingulate cortex. Region-specific laminar patterns characterized (1) motor areas where a lower density in layer III contrasted with the clusters of DA axons in the same layer; (2) the primary visual cortex (area 17), where two bands of higher density in layers III-IV and layer V outlined a poorly innervated zone in layer IVc-beta; (3) the peristriate area 18, where the 5-HT network was relatively loose but with a denser band in layer III. Thus, DA innervation of the cerebral cortex displays major differences between rodents and primates, characterized by expanded cortical targets and by a highly differentiated laminar distribution.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Facilitation of focal cobalt-induced epilepsy after lesions of the noradrenergic locus coeruleus system.

In this study we analyzed the electrophysiological and clinical effects of selective removal of the forebrain noradrenergic projection from the locus coeruleus, induced by bilateral injections of 6-hydroxydopamine into the dorsal tegmental bundle on focal cobalt-induced epilepsy. Noradrenaline depletion caused a marked potentiation of the epilepsy by increasing the duration and intensity of both the clinical and electrophysiological epileptic parameters: epileptic discharges and myoclonic jerks started earlier; spiking and clinical activity were facilitated; duration of the epileptic syndrome was prolonged. On the basis of the present and previous results it is proposed that the ascending noradrenergic system plays a modulatory role on the spread of paroxysmal activities and on the severity of cobalt-induced epilepsy.

Animals↗

Immunocytochemical localization and morphology of GABA-containing neurons in the prefrontal and frontoparietal cortex of the rat.

The distribution and morphology of gamma-aminobutyric acid (GABA)-containing neurons in the rat prefrontal, frontal and parietal cortex were examined using a specific polyclonal antiserum directed against GABA and the immunoperoxidase method. The reaction product was present in the cell bodies, as well as in terminals and some processes without using colchicine. The immunoreactive neurons were observed in all layers but their laminar distribution was different in each cortical area. The immunoreactive cells were more numerous: in layer II and layer V-VI of the frontal cortex, in the deep layers (IV, V, VI) of the parietal cortex and in layer II and layer VI of the prefrontal cortex. The neurons displaying a labelling both in perikarya and processes were classified as multipolar and bipolar neurons. We distinguished various subtypes in each category. Multipolar neurons: cells with a large round soma and thin dendrites radiating in all directions; small neurons with ovoid or angular soma; large neurons with multiangular soma; neurons with a piriform soma. Bipolar neurons: horizontal bipolar cells with ovoid soma and vertical bipolar neurons with fusiform soma.

Animals↗

Major dopamine innervation of the cortical motor areas in the cynomolgus monkey. A radioautographic study with comparative assessment of serotonergic afferents.

Dopamine (DA) and serotonin (5-HT) innervations were revealed by radioautography in primary motor, premotor and supplementary motor (SMA) cortex in Cynomolgus monkeys, using uptake of tritiated amines in vibratome sections under specific conditions that were previously established. DA and 5-HT axons were distributed throughout all cortical layers. A denser DA innervation was found in layers I, III and to a lesser extent layer V with a striking cluster-like arrangement in layer III, particularly in the SMA. 5-HT axons appeared less numerous; their lower density in comparison with DA axons was especially apparent in layer III, particularly in the premotor and motor areas. A DA-5-HT complementarity was thus suggested in this layer. These results suggest that in addition to the motor control exerted through the nigrostriatal pathway, the cortical DA projections could directly modulate the neuronal activity in motor areas. This could be of major importance in the pathophysiology of motor disorders such as Parkinson's disease.

Animals↗

Role of noradrenergic ascending system in extinction of epileptic phenomena.

This chapter reviews results which show that in electroshock-induced and chemically induced convulsions, audiogenic seizures of genetic epilepsy-prone rats and mice, in the kindling focus and the cobalt lesion seizure, susceptibility is modulated by a noradrenergic mechanism. In general, mechanisms that increase or decrease norepinephrine activities decrease or increase seizures, respectively, in these models. In the kindling phenomenon, since the seizure itself provokes an increase in norepinephrine (NE) turnover, with decreased beta-adrenoceptor binding and hyposensitivity to ionophoretic catecholamine application, down regulation could be the cause of hyperexcitability or a consequence of it. In the cobalt focus, supersensitivity to NE appeared when NE-containing terminal density decreased (denervation supersensitivity) and beta-receptor sites increased greater than 50%. Perfusion experiments with NE support the hypothesis that the cortical NE system inhibits the spread of chronic epileptogenic activities in the cobalt focus. In the quaking mouse and in the tottering mouse, noradrenergic dysfunction underlying epileptogenesis may be expressed as a hyperinnervation.

Afferent Pathways↗

Chronic cobalt-induced epilepsy: noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex.

Several studies indicate that brain noradrenaline (NA) depletion facilitates the occurrence of epileptogenic syndromes in various animal models. In cobalt-induced epilepsy in the rat activity is associated with a cortical NA denervation. In order to search for cortical adrenoceptor modifications, inonophoretic studies and adrenoceptor binding assays were performed. At the period of maximal seizure activity, there was a significant supersensitivity of cortical neurons to the ionophoretic application of NA. An increase in the density of beta-adrenoceptor binding sites was observed. No modification in alpha 1- and alpha 2-adrenoceptor binding sites was found. This suggests that in cobalt-induced epilepsy there is a denervation supersensitivity which rests on a selective involvement of beta-adrenoceptors.

Animals↗

Alterations of noradrenaline and serotonin uptake and metabolism in chronic cobalt-induced epilepsy in the rat.

The high affinity uptake of noradrenaline and serotonin, and the concentrations of these monoamines and their metabolites, have been measured in the perifocal cortical area at various stages of the evolution of cobalt-induced epilepsy in the rat. Noradrenaline uptake was maximally reduced at days 8-10 after cortical cobalt application, a time corresponding to the onset of epileptic discharges; it remained diminished during the spiking activity period of the focus (days 14-20) and was back to normal values at day 40, at which time the epileptic syndrome had disappeared. Serotonin uptake was also diminished at days 8-10 but to a lesser extent than was noradrenaline uptake. In the homotopic cerebral cortex contralateral to cobalt application, noradrenaline uptake was reduced at day 10 only and to a lesser extent than in the perifocal area, whereas serotonin uptake was unaffected. Kinetic analysis of the cobalt-induced monoamine uptake alterations at day 10 revealed a diminution of the maximal velocity with no change in the Km. Noradrenaline and dihydroxyphenylethyleneglycol concentrations in the perifocal area were also maximally reduced at days 8-10 but were unaffected at day 2 and day 40 post cobalt application. A reduction of serotonin levels in the perifocal area was observed only at days 8-10 while 5-hydroxyindoleacetic acid remained unaffected throughout the time period studied. The levels of these monoamines and their metabolites were unchanged in the homotopic contralateral cortex 2-40 days after cobalt application. These results indicate that cortical cobalt application induces alterations of the biochemical indices of the density of noradrenaline-containing terminals that closely parallel the evolution of the epileptic syndrome. These data further emphasize the important role of the cortical noradrenergic system in cobalt-induced epilepsy.

Animals↗