Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and pathological data of ten patients with gliomatosis cerebri are compared with 48 well documented cases from the literature. The most striking clinical findings were behavioural and mental changes, seizures, motor weakness and headaches. Though diagnostic techniques have gained in sophistication, the clinical diagnosis of gliomatosis cerebri remains difficult. Laboratory and radiograph tests are mostly unconclusive. Expectations that computed tomography might lead to an accurate diagnosis were not fulfilled. Histological examination disclosed a diffuse proliferation of glial elements infiltrating normal nervous tissue with destruction of myelin sheaths, but only slight damage to neurons and axons. In two cases, areas typical of oligodendroglioma were also present. Glial fibrillary acidic protein staining showed in seven cases that most of the neoplastic cells were of astrocytic origin. In addition, GFAP negative neoplastic cells with the appearance of oligodendroglia and intermediate elements between astroglia and oligodendroglia and irregularly shaped naked nuclei of unidentified nature were found. On the basis of the two-stage theory of carcinogenesis, it is suggested that this disease might be the result of propagation of initiated glial elements which have not yet undergone the process of tumor conversion.
 ...
PMID:Gliomatosis cerebri: clinical and histological findings. 405 56

Stargazer mutant mice inherit a recessive neuronal excitability phenotype featuring frequent non-convulsive spike-wave seizures that arise from synchronous bursting in neocortical, thalamic and hippocampal networks. Immunocytochemistry reveals that granule cells in the mutant dentate gyrus aberrantly express neuropeptide Y (NPY) at multiple ages following the developmental onset of seizures. The ectopic NPY is selectively concentrated in the mossy fibers, co-localizing with the releasable dense core vesicle pool. The NPY content of native NPY+local circuit neurons is also elevated in the mutant CNS. There is no concurrent elevation of hippocampal 72 kDa heat shock protein (HSP72), glial fibrillary acidic protein (GFAP) or NADPH-diaphorase, three markers that are induced during cellular injury, and no evidence of granule cell loss. Since mossy fiber NPY expression appears after the developmental onset of spike-wave discharges and can be induced in wild type granule cells by electrical stimulation, the altered peptide phenotype is likely to reflect transynaptic gene induction triggered by synchronous bursting. These results link a specific pattern of repetitive synaptic input with selective molecular plasticity in dentate granule cells that may contribute to dynamic modifications in hippocampal network excitability.
 ...
PMID:Aberrant expression of neuropeptide Y in hippocampal mossy fibers in the absence of local cell injury following the onset of spike-wave synchronization. 747 19

Expression patterns of cathepsin D (lysosomal aspartic protease) and glial fibrillary acidic protein (GFAP, a marker of reactive astroglia) were determined by Northern blot analysis and immunohistochemistry in the rat brain during neurodegeneration accompanying kainate-evoked seizures. The level of cathepsin D mRNA in the hippocampus, limbic cortex, and temporo-parieto-occipital neocortex was shown to increase, starting at 6 h after kainate treatment, and reaching peak values at 3-7 days after the neurotoxin administration. A similar time course of elevated accumulation was noted for GFAP mRNA in these structures. Immunohistochemical analysis performed 3 days after kainate treatment showed that the increased cathepsin D levels were confined mainly to the degenerating neurons in the susceptible brain areas, while the elevated GFAP immunoreactivity was observed in reactive astrocytes. Although cathepsin D and GFAP expression levels were elevated by kainate administration, their expression patterns revealed significant differences with regard to both intensity and site of induction.
 ...
PMID:Elevated cathepsin D expression in kainate-evoked rat brain neurodegeneration. 758 34

Cytokines are thought to be important mediators in physiologic and pathophysiologic processes affecting the central nervous system (CNS). To explore this hypothesis, transgenic mice were generated in which the cytokine interleukin 6 (IL-6), under the regulatory control of the glial fibrillary acidic protein gene promoter, was overexpressed in the CNS. A number of transgenic founder mice and their offspring exhibited a neurologic syndrome the severity of which correlated with the levels of cerebral IL-6 expression. Transgenic mice with high levels of IL-6 expression developed severe neurologic disease characterized by runting, tremor, ataxia, and seizure. Neuropathologic manifestations included neuro-degeneration, astrocytosis, angiogenesis, and induction of acute-phase-protein production. These findings indicate that cytokines such as IL-6 can have a direct pathogenic role in inflammatory, infectious, and neurodegenerative CNS diseases.
 ...
PMID:Neurologic disease induced in transgenic mice by cerebral overexpression of interleukin 6. 769 79

Previous studies have revealed that kindled seizures induced via chronically implanted electrodes up-regulate the expression of glial fibrillary acidic protein (GFAP), the protein constituent of intermediate filaments in astrocytes. The present study evaluates the consequences of a single electroconvulsive seizure (ECS) on glial gene expression. ECS were induced in mice via externally-placed electrodes. GFAP mRNA levels were evaluated 1, 2, 4, and 6 days post-seizure by in situ hybridization. GFA immunocytostaining was evaluated in a separate series of animals. Following a single ECS, the levels of mRNA for GFAP increased several fold by 1 day and were still substantially elevated at 4 days. The increases occurred primarily in the dentate gyrus despite the fact that the seizures involved widespread brain regions. GFAP mRNA levels were also increased in areas bordering the ventricles, especially in areas immediately adjacent to the dentate gyrus. These results indicate that ECS up-regulates the mRNA for a key structural protein of astrocytes in a manner that is similar to the response that occurs following injury, that this response occurs selectively in a part of the brain that plays a key role in memory function, and that the increase may be due in part to a diffusible substance that also affects glial gene expression in nearby structures.
 ...
PMID:Electroconvulsive seizures upregulate astroglial gene expression selectively in the dentate gyrus. 780 20

Status epilepticus induced by pilocarpine in rats induces massive tissue damage comprising neurons and astrocytes (incomplete infarction) in substantia nigra pars reticulata (SNR) and in basal cortical areas (BCTX). Immunohistochemistry with a polyclonal antiserum and a monoclonal antibody to GFAP were used here to study the astroglial damage in these regions. Control sections showed a strong labeling for glial fibrillary acidic protein (GFAP) for both antibodies in SNR and BCTX. At 1 day after induction of seizures, labeling with the polyclonal antibodies showed diffuse increase within the lesioned areas and enhanced staining of astrocytes at the border zones. However, staining with the monoclonal antibody was abolished. At 3 days, labeling with both the polyclonal antiserum and the monoclonal antibody was severely reduced within the damaged regions. Reactive astrocytes in the surround of the infarct showed enhanced labeling with both antibodies. This combination of enhanced labeling with polyclonal antibodies and decreased labeling with the specific monoclonal antibody for GFAP can be taken as indicator for acute glial cell damage in seizures and related experimental conditions.
 ...
PMID:Loss of immunoreactivity for glial fibrillary acidic protein (GFAP) in astrocytes as a marker for profound tissue damage in substantia nigra and basal cortical areas after status epilepticus induced by pilocarpine in rat. 785 85

Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased epileptogenic activity of the limbic type in a dose-dependent fashion. The KA injection also led to a neuronal cell death and a gliosis, closely correlated to the extent of seizure activity. In biopsies from human epileptogenic cortex, the concentration of neuron specific enolase correlated inversely to that of glial fibrillary acidic protein, a marker for astrocytic glial cells. Stimulation of the KA receptor decreased the extent of phosphorylation of the largest subunit of neurofilaments (NF-H) that have consequences for structural stability and axonal transport. Phosphorylated NF-H decreased also in human epileptic cortex, indicating either an overactivity of excitatory neurotransmitters or a loss of axonal compartments.
 ...
PMID:Excitotoxicity. Experimental correlates to human epilepsy. 788 4

A case of oligodendroglial hamartoma is reported in a 39-year-old man with a 20-year history of petit mal seizures. Magnetic Resonance Imaging of the brain showed a small focal area of abnormal decreased signal on T1-weighted images of the right temporal lobe. The patient became seizure free after the removal of the lesion and treatment with carbamazepine. Pathologic examination revealed several aggregates of oligodendroglial cells with small, dark, regularly stained nuclei and a clear, well-defined perinuclear halo; there was no mixture of neurons or astrocytes. Although these cells were negative, the background was strongly positive for glial fibrillary acidic protein, and myelin basic protein. The histopathologic diagnosis of the temporal lobe lesion was oligodendroglial hamartoma. This report documents an additional subtype of temporal lobe hamartoma associated with seizure disorder.
 ...
PMID:Oligodendroglial hamartoma of the right temporal lobe: a case report and discussion of possible histogenesis. 795 66

The present study evaluates the relative roles of seizure activity and spreading depression in upregulating glial fibrillary acidic protein (GFAP) mRNA expression. Stimulating electrodes were placed bilaterally in the angular bundle, and recording electrodes were placed bilaterally in the dentate gyrus of adult rats. Intense electrographic seizures were induced by delivering stimulus trains through one stimulating electrode. In some cases, spreading depression accompanied the seizures, while in other cases, the seizures occurred in the absence of spreading depression. Animals were killed 24 h following the last stimulus train, and the forebrains were prepared for quantitative in situ hybridization. Seizure activity and spreading depression led to significant increases in GFAP mRNA levels in the hippocampal formation. Seizure activity alone (without spreading depression) induced a 4-fold increase in GFAP mRNA levels in the hilus and molecular layer of the dentate gyrus and in stratum lacunosum-moleculare of the hippocampus. When seizure activity was accompanied by spreading depression, there was a 10-fold increase in GFAP mRNA levels in these same regions. Regional differences within the hippocampal formation in glial cell response were evident. While GFAP mRNA levels in stratum lacunosum-moleculare of the hippocampus were upregulated by seizure activity and spreading depression, levels in hippocampal stratum radiatum of the hippocampus remained unchanged. The results suggest that abnormal neuronal activity can influence glial cell gene expression and that spreading depression is a stronger signal than seizure activity in upregulating GFAP mRNA levels.
 ...
PMID:Spreading depression and reverberatory seizures induce the upregulation of mRNA for glial fibrillary acidic protein. 806 84

We have recently demonstrated that electrically induced seizures lead to dramatic increases in mRNA for GFAP in areas in which seizures occur. The present study evaluates the time course of the changes in the GFAP-mRNA levels after seizures and the relationship between these changes and GFAP protein levels to understand the role of neuronal activity in regulating glial gene expression. GFA protein and mRNA levels were measured in hippocampi from rats in which seizures were induced by: (1) 50-Hz stimulus trains delivered 12 times over the course of 1 day via indwelling electrodes implanted chronically in the CA3 region of the hippocampus; and (2) intraperitoneal injections of pentylenetetrazol. In the case of the electrically induced seizures, we also compared the glial response in animals that had never experienced a seizure with the response in animals that previously had been kindled but had not experienced a seizure for 30 days. Electrically induced seizures led to rapid transient increases in GFAP-mRNA levels in the hippocampus ipsi- and contralateral to the stimulation. GFAP-mRNA increased about five-fold 1 day after the end of seizure activity and returned to near-control levels by 4 days. There were no detectable increases in GFA protein at 1 day but by 2 days GFA protein levels had increased about two-fold. GFA protein levels remained elevated until 4 days poststimulation and then began to decrease. The responses were similar when seizures were induced in kindled animals, except that the GFAP protein levels remained elevated for somewhat longer.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Glial response to neuronal activity: GFAP-mRNA and protein levels are transiently increased in the hippocampus after seizures. 813 Oct 53


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>