Showing results 41 to 51 of 51
   Partial Cloning and Distribution of Estrogen Receptor Beta in the Avian BrainLakaye, Bernard  ; Foidart, Agnès ; Grisar, Thierry et alin Neuroreport (1998), 9(12), 2743-8 A partial estrogen receptor beta (ER-beta) cDNA was isolated from testicular quail RNA by RT-PCR with degenerate primers specific to the rat ER-beta sequence. A high expression of ER-beta was demonstrated ... [more ▼] A partial estrogen receptor beta (ER-beta) cDNA was isolated from testicular quail RNA by RT-PCR with degenerate primers specific to the rat ER-beta sequence. A high expression of ER-beta was demonstrated by RT-PCR in the telencephalon, diencephalon, pituitary, testis and kidneys of male quail but little or no expression was detected in the cerebellum, pectoral muscle and adrenal gland. In situ hybridization with a 35S-labelled oligoprobe in sections through the preoptic area-rostral hypothalamus identified high expression in the medial preoptic nucleus, bed nucleus striae terminalis and nucleus taeniae. These data demonstrate the presence of an ER-beta in brain areas implicated in the control of reproduction in a non-mammalian species. [less ▲] Detailed reference viewed: 13 (1 ULg) Cloning of the Rat Brain Cdna Encoding for the Slc-1 G Protein-Coupled Receptor Reveals the Presence of an Intron in the GeneLakaye, Bernard ; Minet, Arlette ; Zorzi, Willy et alin Biochimica et Biophysica Acta (1998), 1401(2), 216-20 In order to isolate new G protein-coupled receptors expressed in the cerebral cortex, a set of degenerate oligonucleotides corresponding to the third and seventh transmembrane segment were synthetized ... [more ▼] In order to isolate new G protein-coupled receptors expressed in the cerebral cortex, a set of degenerate oligonucleotides corresponding to the third and seventh transmembrane segment were synthetized. Their use in PCR on rat brain cortex mRNA amplified several cDNA fragments. One of them, a 526 bp sequence, encoded for what was at that time an unknown G protein-coupled receptor. An oligonucleotide derived from the sequence was then used as a probe to isolate the receptor cDNA from a rat brain cDNA library. It encodes for a 353aa protein with seven transmembrane segments, three consensus N-glycosylation sites at the amino terminus and several potential phosphorylation sites in the intracellular loops. This protein shares 91% overall identity with a recently cloned human somatostatin-like receptor of 402aa named SLC-1. This suggests that we have cloned the rat orthologue of the human SLC-1. However, the extracellular N-terminus of the human receptor is 49 amino acids longer and shows 50% identity with the rat one. Because the human sequence was deduced from genomic DNA, we suspected the presence of an intron in the gene. This was confirmed by PCR using primers spanning the intron. On the basis of the sequence of a 128 kb fragment of chromosome 22 encompassing the SLC-1 gene, we were able to deduce a corrected amino acids sequence for the human receptor. So both rat and human SLC-1 receptors are 353aa long, with three consensus N-glycosylation sites. They share 96% identity at the amino acid level and are encoded by a gene containing one intron in the coding sequence. [less ▲] Detailed reference viewed: 11 (1 ULg)Low Thiamine Diphosphate Levels in Brains of Patients with Frontal Lobe Degeneration of the Non-Alzheimer's TypeBettendorff, Lucien ; ; et alin Journal of Neurochemistry (1997), 69(5), 2005-2010 We compared the thiamine and thiamine phosphate contents in the frontal, temporal, parietal, and occipital cortex of six patients with frontal lobe degeneration of the non-Alzheimer's type (FNAD) or ... [more ▼] We compared the thiamine and thiamine phosphate contents in the frontal, temporal, parietal, and occipital cortex of six patients with frontal lobe degeneration of the non-Alzheimer's type (FNAD) or frontotemporal dementia with five age-, postmortem delay-, and agonal status-matched control subjects. Our results reveal a 40-50% decrease in thiamine diphosphate (TDP) in the cortex of FNAD patients, whereas thiamine monophosphate was increased 49-119%. TDP synthesizing and hydrolyzing enzymes were unaffected. The activity of citrate synthase, a mitochondrial marker enzyme, was decreased in the frontal cortex of patients with FNAD, but no correlation with TDP content was found. These results suggest that decreased contents of TDP, which is essentially mitochondrial, is a specific feature of FNAD. As TDP is an essential cofactor for oxidative metabolism and neurotransmitter synthesis, and because low thiamine status (compared with other species) is a constant feature in humans, a nearly 50% decrease in cortical TDP content may contribute significantly to the clinical symptoms observed in FNAD. This study also provides a basis for a trial of thiamine, to improve the cognitive status of the patients. [less ▲] Detailed reference viewed: 18 (1 ULg)Molecular Basis of Neuronal Biorhythms and ParoxysmsGrisar, Thierry ; Lakaye, Bernard ; in Archives of Physiology & Biochemistry (1996), 104(6), 770-4 The molecular basis of the biorhythms are evoked in relation to cerebral EEG rhythms and paroxysms. Basic oscillatory phenomena have been well shown and modeled in systems such as the glycolytic pathway ... [more ▼] The molecular basis of the biorhythms are evoked in relation to cerebral EEG rhythms and paroxysms. Basic oscillatory phenomena have been well shown and modeled in systems such as the glycolytic pathway, the oscillations of cAMP in amoebas and rhythms of the intracellular cycline during mitosis. In excitable cells the intracellular calcium and cAMP oscillations exhibit a signalling system with many advantages. Thus the question arises: to what extent can the EEG paroxysms observed in epileptic syndrome be due to disturbances in such basic molecular pathways that underlie intracellular molecular oscillations? The usefulness of the absence-rat-model and the implication the T type Ca(2+)-channel of the thalamic nuclei in the pathophysiology of this epileptic syndrome are discussed. [less ▲] Detailed reference viewed: 17 (2 ULg)Thiamine, Thiamine Phosphates, and Their Metabolizing Enzymes in Human BrainBettendorff, Lucien ; ; et alin Journal of Neurochemistry (1996), 66(1), 250-8 Total thiamine (the sum of thiamine and its phosphate esters) concentrations are two- to fourfold lower in human brain than in the brain of other mammals. There were no differences in the total thiamine ... [more ▼] Total thiamine (the sum of thiamine and its phosphate esters) concentrations are two- to fourfold lower in human brain than in the brain of other mammals. There were no differences in the total thiamine content between biopsied and autopsied human brain, except that in the latter, thiamine triphosphate was undetectable. The main thiamine phosphate-metabolizing enzymes could be detected in autopsied brain, and the kinetic parameters were comparable to those reported in other species. Thiamine diphosphate levels were lowest in hippocampus (15 +/- 4 pmol/mg of protein) and highest in mammillary bodies (24 +/- 4 pmol/mg of protein). Maximal levels of thiamine and its phosphate ester were found to be present at birth. In parietal cortex and globus pallidus, mean levels of total thiamine in the oldest age group (77-103 years) were, respectively, 21 and 26% lower than those in the middle age group (40-55 years). Unlike cerebral cortex, the globus pallidus showed a sharp drop in thiamine diphosphate levels during infancy, with concentrations in the oldest group being only approximately 50% of the levels present during the first 4 months of life. These data, consistent with previous observations conducted in blood, suggest a tendency toward decreased thiamine status in older people. [less ▲] Detailed reference viewed: 16 (1 ULg)Brain thiamine, its phosphate esters, and its metabolizing enzymes in Alzheimer's disease.; Bettendorff, Lucien ; Grisar, Thierry et alin Annals of Neurology (1996), 39 Detailed reference viewed: 5 (1 ULg) Thiamine Deficiency--Induced Partial Necrosis and Mitochondrial Uncoupling in Neuroblastoma Cells Are Rapidly Reversed by Addition of ThiamineBettendorff, Lucien ; Sluse, Francis ; Goessens, Guy et alin Journal of Neurochemistry (1995), 65(5), 2178-2184 Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the ... [more ▼] Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled, and their cristae are disorganized. Glutamate formed from glutamine is no longer oxidized and accumulates, suggesting that the thiamine diphosphate-dependent alpha-ketoglutarate dehydrogenase activity is impaired. When thiamine (10 microM) is added to the cells, the O2 consumption increases, respiratory control is restored, and normal cell and mitochondrial morphology is recovered within 1 h. Succinate, which is oxidized via the thiamine diphosphate-independent succinate dehydrogenase, is also able to restore a normal O2 consumption (with respiratory control) in digitonin-permeabilized thiamine-deficient cells. Our results therefore suggest that the slowing of the citric acid cycle is the main cause of the biochemical lesion induced by thiamine deficiency as observed in Wernicke's encephalopathy. [less ▲] Detailed reference viewed: 38 (23 ULg)Thiamine Deficiency in Cultured Neuroblastoma Cells: Effect on Mitochondrial Function and Peripheral Benzodiazepine ReceptorsBettendorff, Lucien ; Goessens, Guy ; Sluse, Francis et alin Journal of Neurochemistry (1995), 64(5), 2013-2021 When neuroblastoma cells were transferred to a medium of low (6 nM) thiamine concentration, a 16-fold decrease in total intracellular thiamine content occurred within 8 days. Respiration and ATP levels ... [more ▼] When neuroblastoma cells were transferred to a medium of low (6 nM) thiamine concentration, a 16-fold decrease in total intracellular thiamine content occurred within 8 days. Respiration and ATP levels were only slightly affected, but addition of a thiamine transport inhibitor (amprolium) decreased ATP content and increased lactate production. Oxygen consumption became low and insensitive to oligomycin and uncouplers. At least 25% of mitochondria were swollen and electron translucent. Cell mortality increased to 75% within 5 days. [3H]PK 11195, a specific ligand of peripheral benzodiazepine receptors (located in the outer mitochondrial membrane) binds to the cells with high affinity (KD = 1.4 +/- 0.2 nM). Thiamine deficiency leads to an increase in both Bmax and KD. Changes in binding parameters for peripheral benzodiazepine receptors may be related to structural or permeability changes in mitochondrial outer membranes. In addition to the high-affinity (nanomolar range) binding site for peripheral benzodiazepine ligands, there is a low-affinity (micromolar range) saturable binding for PK 11195. At micromolar concentrations, peripheral benzodiazepines inhibit thiamine uptake by the cells. Altogether, our results suggest that impairment of oxidative metabolism, followed by mitochondrial swelling and disorganization of cristae, is the main cause of cell mortality in severely thiamine-deficient neuroblastoma cells. [less ▲] Detailed reference viewed: 19 (9 ULg)An Atypical Anion Transporter Functioning at Acid pH in Neuroblastoma CellsBettendorff, Lucien ; ; et alin Biochemical and Biophysical Research Communications (1995), 207(1), 375-381 At pH 7.4, 36Cl- uptake by neuroblastoma cells was Na(+)-independent, saturable and blocked by submicromolar concentrations of DIDS. This suggests that at this pH, Cl- transport is mediated by an ... [more ▼] At pH 7.4, 36Cl- uptake by neuroblastoma cells was Na(+)-independent, saturable and blocked by submicromolar concentrations of DIDS. This suggests that at this pH, Cl- transport is mediated by an exchanger analogous to erythroid band 3. At pH 6. [less ▲] Detailed reference viewed: 12 (7 ULg)Contribution of Positron Emission Tomography to the Investigation of Epilepsies of Frontal Lobe OriginFranck, Georges ; Maquet, Pierre ; Sadzot, Bernard et alin Advances in Neurology (1992), 57 Detailed reference viewed: 7 (1 ULg)Cerebral ischemic accidents in young patients, less than 45 years of age; ; Grisar, Thierry et alin Semaine des Hôpitaux de Paris. Thérapeutique (1983), 59(37-38), 2642-2644 Detailed reference viewed: 6 (1 ULg) |
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