Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal necrosis in the brain resulting from status epilepticus of 15 to 120 minutes duration in ventilated and well-oxygenated rats was assessed. Seizures were induced by inhalation of the convulsant gas flurothyl, and terminated by withdrawal of flurothyl and a single injection of thiopental. The animals were allowed to recover for one week, and neuronal damage was assessed by cell counts following subserial sectioning of the brain and microscopical examination of the sections. Infarction of the pars reticulata of the substantia nigra occurred in 5 of the 6 animals with seizure duration of 30 minutes, and in all animals with longer seizure durations. There also was a common affectation of the central parts of the globus pallidus. The pars compacta of the substantia nigra was never affected. After 45 to 120 minutes of seizures, moderate neuronal necrosis was observed in the neocortex (layers 3 and 4), and after 60 to 120 minutes was seen in amygdaloid and thalamic nuclei, as well as in CA4 and CA1 hippocampal pyramidal cells. Notably, CA3 neurons were not damaged nor were dentate granule cells affected. After 120 minutes of seizures, damage regularly affected the neocortex and the ventral-posterior nuclei of the thalamus. A conspicuous feature was the localization of neuronal necrosis at sites close to the ventricles.
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PMID:Status epilepticus in well-oxygenated rats causes neuronal necrosis. 405 57

Light and electron microscopy (with the combined oxalate-pyroantimonate technique for the electron microscopic visualization of intracellular calcium) were used to compare the hippocampal pathology in rats killed immediately after 1.5-2 h of L-allylglycine-induced seizures with that in rats allowed 15-60 min of a seizure-free "recovery" period before perfusion fixation. Following 1.5 h of seizure activity, cellular pathology included astrocytic swelling and dark cell degeneration of pyramidal and polymorphic neurons. This was accompanied by a marked increase in the amount of calcium pyroantimonate deposits, particularly in swollen and disrupted mitochondria of CA1 and CA3 basal dendrites and in certain neuronal cell bodies in the CA1 and CA3 regions and the hilus. After a seizure-free period of between 30 and 60 min the hippocampi showed almost complete recovery except for a few remaining dark, shrunken cells. The majority of these were presumed to be interneurons. The ultrastructural changes were consistent with the observations by light microscopy. By 60 min, excess calcium deposits had disappeared except in the dark cells in which intracellular vacuoles retained deposits. We conclude that most of the pathological changes observed after 1.5 h of L-allylglycine induced status epilepticus, including the mitochondrial calcium "overload" are reversible. At 1 h after termination of status epilepticus apparently irreversible pathology (dark cell change, "ischaemic cell change") concerns predominantly the polymorphic neurons.
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PMID:Status epilepticus: the reversibility of calcium loading and acute neuronal pathological changes in the rat hippocampus. 646 62

Systemic injections of kainic acid (KA) in adult rats rapidly induce sustained motor seizures preferentially involving the limbic structures and culminating in status epilepticus. The hippocampal formation and amygdala seem to occupy a central position for the onset of paroxysmal discharge and for the manifestation of limbic signs respectively. With long survival periods, the animals spontaneously display limbic motor seizures and a second administration of KA produces more severe effects. The brain damage, found in several limbic structures subsequent to KA-induced seizures, is reminiscent of that seen in human epileptics, and electrographical and metabolic studies (using the 2-deoxyglucose method) reveal that it follows increased neuronal and metabolic activation. The crucial role of the mossy fiber system in the particular vulnerability to KA of the CA3 neurons of Ammon's horn is also suggested by a study of the maturation of the KA-induced seizure and brain damage syndrome.
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PMID:Usefulness of parenteral kainic acid as a model of temporal lobe epilepsy. 652 79

Using electron microscopy and the combined oxalate-pyroantimonate technique, free calcium ions were located in the hippocampus of control rats and of those that had undergone status epilepticus induced by L-allylglycine or bicuculline. The validity of this technique was established by the use of the calcium chelating agent ethylene glycol bis(beta-aminoethyl ether), N,N'-tetra-acetic acid and by an X-ray microanalytical technique. In control material, calcium deposits were visible in synaptic vesicles and multivesicular bodies, in parts of the Golgi apparatus, mitochondria, lysosomes, and in glial and neuronal nuclei. Following 2 h of status epilepticus, cellular pathology included astrocytic swelling, and dark cell degeneration of pyramidal neurons. This was accompanied by a marked increase in the amount of calcium pyroantimonate deposits, particularly in swollen and disrupted mitochondria of CA1 and CA3 basal dendrites, and in selected neuronal cell bodies in the CA1 and CA3-4 regions. We propose that enhanced calcium entry into neurons and consequent overloading of the capacity of mitochondria for calcium sequestration is part of the cytotoxic mechanism leading to selective neuronal loss in the hippocampus in status epilepticus.
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PMID:Intracellular calcium accumulation in rat hippocampus during seizures induced by bicuculline or L-allylglycine. 663 67

Status epilepticus was induced in thirteen paralysed and ventilated rats by the injection of either bicuculline or L-allylglycine. After 1-2 h of seizure activity the animals were intracardially perfused with a 2% glutaraldehyde/3% paraformaldehyde solution. Hippocampal blocks from each rat were processed for light and electron microscopy. The effects of L-allylglycine were more severe than those of bicuculline. Changes include perivascular and perineuronal swelling of astrocytic processes, and neuronal alterations which were graded as follows: Grade I (least severe), neuronal cytoplasm appears slightly darker than usual; Grade II, condensed or dark neurons, usually with microvacuoles; and Grade III classical 'ischaemic cell change'--the cytoplasm and karyoplasm is dark and shrunken, with or without microvacuoles. Many of the microvacuoles originate from mitochondria. In a few cases swollen and disrupted mitochondria are also seen is distended basal dendrites of the CA3 and CA1 pyramidal neurons. Dentate granule cells appear unaffected. The hippocampal neuronal alterations induced by seizure activity include those of 'ischaemic cell change'. The pathogenetic factors common to hypoxia/ischaemia and status epilepticus remain to be identified.
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PMID:Early changes in the rat hippocampus following seizures induced by bicuculline or L-allylglycine: a light and electron microscope study. 684 75

Taber et al. (1977) introduced new model of epilepsy to obtain experimental status epilepticus in mice, through a modification of the kindling method (Goddard et al. 1969). The aim of this paper is to report the effect of Taber's modification on a new animal specie (rats). Bipolar, twisted steel electrodes were stereotaxically implanted into the CA1-CA3 regions of the dorsal hippocampus. After one week the animals received 2 h stimulation sessions, one stimulus per minute, during which a sustained electrographical and behavioral seizures were induced. Different patterns of electrographical discharges as well as tonic-clonic convulsions were observed. The animals which were submitted to 3 stimulating sessions respectively 7, 14 and 21 days after surgery showed an increase in the epileptic activity. This has been interpreted as a plastic neural modification of the hippocampus similar to that observed during learning and memory consolidation. In comparison to other inducing kindling methods this one permits a more rapid elicitation of the phenomenon. For this reason this method will provide a good epilepsy model for the study of anticonvulsant drugs and basic mechanisms involved in the epileptic activity.
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PMID:[Modification of the "kindling" method for obtaining experimental status epilepticus in rats]. 699 53

Using electron microscopy and the combined oxalate--pyroantimonate technique, calcium was located in hippocampal neurons of rats that had undergone L-allylglycine-induced status epilepticus. In control material, calcium deposits were prominent in nearly every synaptic vesicle, and to a lesser degree in mitochondria and the Golgi apparatus of pyramidal neurons and dentate granule cells. After status epilepticus, mitochondrial calcium deposits increased, particularly in the swollen mitochondria of the pyramidal cell bodies and basal dendrites of CA3 and CA1 neurones. These studies support the theory that enhanced calcium entry leading to calcium overload of mitochondria may be an important cytotoxic mechanism producing selective neuronal loss.
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PMID:Intracellular sites of early calcium accumulation in the rat hippocampus during status epilepticus. 711 Jun 39

Despite ready induction of severe limbic status epilepticus by systemic kainic acid (KA) in infant rats, excitotoxic neuronal injury has not been observed. The mechanisms of this resistance of the immature hippocampus to excitotoxicity are unknown. Acid fuchsin stain has been used as a marker of irreversibly injured neurons in the adult brain. We speculated that the dye might map reversibly injured neurons in the infant. Subsequent to KA-induced status epilepticus in 11-day-old rats, acid fuchsin stain was evident in the hippocampal CA3, CA1, dentate gyrus and hilus by 24 h, peaked at 48 h and disappeared by 6 days, without evidence for neuronal loss. Acid fuchsin may be a useful tool for delineating the distribution of reversibly injured immature neurons in experimental seizure paradigms.
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PMID:Status epilepticus results in reversible neuronal injury in infant rat hippocampus: novel use of a marker. 751 May 87

In the present investigation we address the question of whether one of the responses to increased neuronal activity is a modification of the expression of the different subunits of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)-selective glutamate receptors (GluR-1, GluR-2, GluR-3). Thus, we used two different models of generalized status epilepticus, as widespread elevated neuronal activity, to study in vivo responses of the AMPA receptor mRNA expression in rat forebrain. By Northern blot analysis and in situ hybridization, we show that one of the delayed responses to LiCl/pilocarpine-induced status epilepticus is a dramatic change in the mRNA level of some subunits of AMPA-selective glutamate receptors. These effects, which appear between 6 and 12 h after the drug treatment, are subunit and brain region specific. The most striking example of differential expression of the three examined GluR mRNAs can be observed in the dentate gyrus of the hippocampus. In this specific brain subregion an increase of GluR-3 mRNA level is induced 12 h after LiCl/pilocarpine treatment, while a clear decrease in GluR-1 mRNA level and no significant change in GluR-2 mRNA level can be observed in the same area under these experimental conditions. Both the GluR-1 decrease and the GluR-3 increase are transient effects and a return to basal level can be observed after 48-72 h. In the CA1 layer of the hippocampus, a parallel decrease of both GluR-1 and GluR-3 expression is found 12-24 h after drug treatment, followed by a recovery of the expression to control values at 48 h. In kainate-induced epilepsy we could reproduce the late increase (12-24 h) in GluR-3 mRNA in the dentate gyrus; however, under this experimental condition, no clear decrease of GluR-1 expression can be observed in this area. A general decrease in mRNA level for the AMPA receptor subunits (GluR-1-3) in the hippocampal layers, in particular in CA3 and CA4 subfields, was also observed. In conclusion the results reported in the present paper reveal a specific regulation of GluR gene expression in the granule cells of the hippocampal dentate gyrus and stimulate further investigation on the functional role of the GluR-3 subunit in the receptor-channel complex.
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PMID:Changes in gene expression of AMPA-selective glutamate receptor subunits induced by status epilepticus in rat brain. 752 10

Adenosine is thought to act as an endogenous anticonvulsant and neuroprotective substance in the brain. In the present study we compared neuronal death following status epilepticus (SE) induced in the presence of 8-cyclopentyl-1,3-dimethylxanthine (8-CPT), an A1-adenosine receptor antagonist, with that following SE induced by continuous hippocampal stimulation. Hippocampal damage was characterized using selective nerve and nonnerve cell markers. Six days after SE, both models produced similar patterns of CA1 and CA3 cell loss and selective loss of parvalbumin and hilar somatostatin-immunoreactive interneurons. Calbindin D28K-immunoreactive interneuron numbers and calbindin D28K immunoreactivity in dentate granule cells remained unchanged although calbindin D28K staining was lost in damaged CA1 neurons. Neuronal injury in these areas was also accompanied by reactive gliosis and microglial proliferation, as well as the production of basic fibroblast growth factor and insulin-like growth factor-1 by astrocytes. Although hippocampal damage appeared to be more severe after SE induced in the presence of 8-CPT, this may be due to the increased severity of SE generated in this model.
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PMID:Neuronal injury following electrically induced status epilepticus with and without adenosine receptor antagonism. 764 19


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