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  • 1
    Electronic Resource
    Electronic Resource
    In Vivo Activation of Kainate Receptors Induces Dephosphorylation of the Heavy Neurofilament Subunit (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Injection of kainic acid (KA) into the rat hippocampus reduced the phosphorylation-related immunoreactivity of the heavy subunit of neurofilament proteins (NF-H). The effect was demonstrated quantitatively with a dot-immunobinding assay and qualitatively by immunoblotting with monoclonal antibodies against phosphorylation-dependent and nonphosphorylation-related epitopes of NF-H. The KA-induced reduction affected 50% of the phosphorylated NF-H in half of the hippocampus after 48 h. At the same time, the nonphosphorylation-related NF-H immunoreactivity increased as revealed by immunoblotting, indicating a shift from phosphorylated to nonphosphorylated NF-H. The effects on NF-H preceeded a decrease in content of the neuron-specific enolase, a soluble neuronal cytoplasmic protein. No alterations of the light subunit of neurofilament proteins occurred, suggesting that KA has a preferential effect on NF-H phosphorylation. N-Methyl-D-aspartate administered similarly did not lead to a rapid dephosphorylation of NF-H. We propose that kainate receptor-mediated dephosphorylation in NF-H is involved in the signal transduction of excitatory amino acids with consequences for neuronal functions dependent on intermediary filament phosphorylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11037.x
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  • 2
    Electronic Resource
    Electronic Resource
    Antisense inhibition of BCL-2 expression induces retinoic acid-mediated cell death during differentiation of human NT2N neurons (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 76 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Changes in expression of the proto-oncogene Bcl-2are well known in the developing brain, with a high expression level in young post-mitotic neurons that are beginning the outgrowth of processes. The physiological significance of the Bcl-2 up-regulation in these neurons is not fully understood. We used a differentiation model for human CNS neurons to study the expression and function of Bcl-2. NT2/D1 human neuronal precursor cells differentiated into a neuronal phenotype in the presence of 10 µm retinoic acid for 3–5 weeks. This concentration of retinoic acid was not toxic to undifferentiated NT2/D1 cells but was sufficient to up-regulate the BCL-2 protein in 6 days. The BCL-2 levels increased further after 3 weeks, i.e. when the cells started to show neuronal morphology. Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. The loss of neuron-like cells from differentiating cultures indicated that the dead cells were those committed to neuronal differentiation. Death was related to the presence of retinoic acid since withdrawal of retinoic acid after 16 days of treatment dramatically increased cell surviving. The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40–80 µm) of retinoic acid. Furthermore, down-regulation of BCL-2 levels by an antisense oligonucleotide in neuronally differentiated NT2/D1 cells increased their susceptibility to retinoic acid-induced apoptosis. These results indicate that one function of the up-regulation of endogenous BCL-2 during neuronal differentiation is to regulate the sensitivity of young post-mitotic neurons to retinoic acid-mediated apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00142.x
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  • 3
    Electronic Resource
    Electronic Resource
    The brain-specific S 100 protein in small cerebral stab wounds in the rat (1976)
    Springer
    Acta neuropathologica 36 (1976), S. 39-45 
    Details
    ISSN: 1432-0533
    Keywords: S 100 ; Cerebral cortex ; Immunoelectrophoresis ; Stab wound ; Brain injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A quantitative study of the changes in water-soluble proteins and water-soluble S 100 was made in stab-wounded rat frontal cortex as compared to unoperated controls. No great changes occurred until 30 days after the injury. At that time there was no change in the amount of water-soluble S 100 protein/g wet weight, but a large decrease in the amount of water-soloble proteins/g wet weight and thus a proportionate increase in the amount of water-soluble S 100 protein/mg of water-soluble proteins. The significance of the results is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685146
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  • 4
    Electronic Resource
    Electronic Resource
    Lipid composition and fatty acid pattern of the gerbil brain after exposure to perchloroethylene (1987)
    Springer
    Archives of toxicology 60 (1987), S. 397-400 
    Details
    ISSN: 1432-0738
    Keywords: Cerebral cortex ; Chronic exposure ; Fatty acid composition ; Fatty acid desaturation ; Gerbil brain ; Hippocampus ; Lipid composition ; Phospholipids ; Perchloroethylene ; Tetrachloroethylene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Continuous inhalation of perchloroethylene (PCE) (320 ppm) for 3 months by Mongolian gerbils resulted in an altered fatty acid pattern of a brain phospholipid. A minor decrease in the brain weight was also observed. In ethanolamine phosphoglyceride of the cerebral cortex and the hippocampus, a decrease was found among the minor fatty acids derived from linolenic acid with a corresponding increase in several fatty acids of the linoleic acid family. Linoleic acid itself was decreased. Stearic acid was also decreased in both the cerebral cortex and the hippocampus. These changes in the fatty acid pattern indicate increased desaturation. PCE might alter the desaturase activity either directly by interfering with the protein moieties of the enzyme system, or indirectly by changing the properties of the lipid matrix. The observed changes in fatty acid composition are also consistent with the current hypothesis that solvents and anesthetics perturb the lipid matrix of membranes, possibly inducing complex compensatory changes in the membrane lipid composition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00295762
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  • 5
    Electronic Resource
    Electronic Resource
    Neuronal and glial marker proteins in encephalopathy associated with acute liver failure and acute hyperammonemia in the rabbit (1993)
    Springer
    Metabolic brain disease 8 (1993), S. 95-106 
    Details
    ISSN: 1573-7365
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neuronal and glial cell marker proteins were quantified in order to evaluate the possibility of increased proteolysis in the brain of rabbits with acute liver failure and acute hyperammonemia. Acute liver failure was induced by a two-stage devascularization procedure. Acute hyperammonemia was induced by a prolonged infusion of ammonium acetate, which simulates the plasma ammonia level in acute liver failure. Control animals received an infusion of sodium/potassium acetate. After development of severe encephalopathy, the animals were sacrificed (13.7 ± 1.3 hours for rabbits with acute liver failure and 20.2 ± 0.8 hours for rabbits with hyperammonemia) (x ± S.E.M./n=6) and their brains were dissected into cerebral cortex, hippocampus, cerebellum and brain stem. The total protein content and the concentrations of the neuronal cell marker proteins NSE (neuron specific enolase), NF68 and NF200 (68 kD and 200 kD neurofilament polypeptides) and the glial cell marker proteins GFAP (glial fibrillary acidic protein) and S-100 were determined. Total protein content was decreased in the brain stem in acute hyperammonemia only. The content of neuronal and glial cell markers was not affected in either of the two conditions. However, low molecular weight proteolytic fragments of the NF 68 kD polypeptide were observed in the hippocampus of three out of six animals in both experimental groups. No proteolytic degradation of GFAP was observed. The results show that, in experimental encephalopathy due to acute liver failure and acute hyperammonemia, no major changes occur in the marker proteins. The finding of proteolytic fragments of the NF68 polypeptide indicates that the neuronal population is affected prior to glial alterations. These findings are in agreement with the concept that acute hepatic encephalopathy is reversible and induces only slight structural changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00996892
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  • 6
    Electronic Resource
    Electronic Resource
    Modulation of ATPase activities in the central nervous system by the S-100 proteins (1989)
    Springer
    Neurochemical research 14 (1989), S. 761-764 
    Details
    ISSN: 1573-6903
    Keywords: S-100a ; S-100b ; Ca2+ ; Zn2+ ; ATPase ; myelin ; synaptosome ; Gerbil brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The isomeric forms of bovine S-100a and S-100b have been shown to stimulate ATPase activities in fractions enriched in myelin and mitochondria isolated from the Gerbil brain and for S-100b more effectively than for calmodulin in erythrocytes or skeletal muscle. In the presence of Ca2+, S-100a produced a slight increase of ATPase activity in the mitochondrial fraction. However, S-100b, with or without Ca2+ and Zn2+ respectively, had no effect on the ATPase activity in mitochondria of the Gerbil liver. The observations may indicate a “second messenger” role for S-100b in the presence of Zn2+ in the Schwann cell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964955
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  • 7
    Electronic Resource
    Electronic Resource
    Proteolysis of filament proteins in glial and neuronal cells afterIn vivo stimulation of hippocampal NMDA receptors (1992)
    Springer
    Neurochemical research 17 (1992), S. 1005-1009 
    Details
    ISSN: 1573-6903
    Keywords: N-methyl-d-aspartate ; glial fibrillary acidic protein ; neurofilament proteins ; rat hippocampus ; immunoblotting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An intrahippocampal injection of N-methyl-D-aspartate induced the appearance of degradation products of both the 68 kiloDalton neurofilament protein and the glial fibrillary acidic protein, as revealed by immunoblot techniques. The degradation of these two filament proteins was maximal at 10 days after the lession. The degradation patterns were similar to those induced with calpains or calcium in vitro. There were no degradation effects on the 200 kD neurofilament protein as tested with both mono- and polyclonal antibodies. Consequently, the neuronal degeneration after excessive activation of NMDA receptors appears to involve calcium activation of proteolytic enzymes. The effects on the glial proteins are probably secondary to neuronal damage but could be related to calcium dependent processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966828
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  • 8
    Electronic Resource
    Electronic Resource
    Biochemical correlates to cortical dysplasia, gliosis, and astrocytoma infiltration in human epileptogenic cortex (1993)
    Springer
    Neurochemical research 18 (1993), S. 511-518 
    Details
    ISSN: 1573-6903
    Keywords: Epilepsy ; human ; temporal cortex ; gliosis ; astrocytoma, mild cortical dysplasia ; neuron specific enolase ; neurofilament polypeptides ; glial fibrillary acidic protein ; S-100 ; neural cell adhesion molecule
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The study provides detailed biochemical correlates to the common histopathological diagnoses in epilepsy. A dot immunobinding procedure was used for quantification of NSE, GFA, S-100, NCAM, NF 68 and NF 200. The material consisted of samples from 48 patients either selected for surgical treatment of partial epilepsy or for disorders not related to epilepsy. The histopthological diagnosis of the epileptic cases was: MCD (mild cortical dysplasia, microdysgenesis), gliosis, astrocytoma, ganglioglioma, oligodendroglioma and single cases. The concentration in non-epileptic white matter, in per cent of that in grey matter was: NSE, 85; GFA, 175; S-100, 117; NCAM, 43; NF 68,227 and NF 200, 173. The concentration of NSE as well as of GFA was close to normal in the specimens of the MCD and gliosis groups and of one subgroup of the astrocytomas. There was a striking inverse relationship of the GFA vs the NSE concentrations in the whole material. The concentrations of S-100 showed no such inverse relationship to NSE levels. In all the epileptic groups, total NCAM was lower than 50% of that of the non-epileptic group. The mean NF 68 and NF 200 concentration in the gliosis and astrocytoma groups was 75% of the of the non-epileptic group while the corresponding value for the MCD group was 50%. There was a positive correlation of immunochemically determined GFA and the histopathological gliosis score in the samples of epileptogenic cortex. There was no correlation between the concentration of GFA in the samples and the duration of epilepsy. The concentration of neuronal markers was relatively unaffected in the cortex of most patients with epilepsy related to MCD, gliosis and even to astrocytoma infiltration, even after years of seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00967255
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