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)

Status epilepticus may be followed by the loss of selectively vulnerable neurons in the hippocampus and neocortex. The acute cytopathology preceding cell loss is that of "ischemic cell change" or "dark cell change." In the hippocampus, selectively vulnerable neurons (CA3 and CA1 pyramidal neurons, hilar polymorphic neurons) show swelling of mitochondria in the perikaryon and dendrites after 30 to 120 min of seizure activity. Electron-microscopic studies with the combined oxalate/pyroantimonate technique reveal dense calcium pyroantimonate deposits in the swollen mitochondria. Suppression of seizure activity for 30 to 60 min is sufficient to allow recovery of normal mitochondrial morphology and calcium load. A small proportion of vulnerable neurons develop ischemic cell change with multiple vacuoles containing calcium pyroantimonate deposits. Neurons prone to burst firing accumulate calcium during seizures, and eventually show massive "overloading" of mitochondria. Although by analogy with studies in muscle a cytotoxic role for raised cytosolic calcium concentration has been proposed, the link between increased [CA2+] activation of phospholipases and proteinases and ischemic cell change remains uncertain.
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PMID:Cell damage in epilepsy and the role of calcium in cytotoxicity. 370 26

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

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

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

The star fruit (Averrhoa carambola) is consumed in high amounts in Asia and Central/South America. It contains oxalic acid and caramboxin. In some individuals, its ingestion may lead to nephrotoxicity and neurotoxicity. The nephrotoxic effect is due to oxalate deposition in renal tubules resulting in acute tubular necrosis and interstitial nephritis. Although uraemic encephalopathy secondary to acute kidney injury may play a role, a shift to an excitatory state of the central nervous system (CNS) by caramboxin through activation of excitatory neuroreceptors and inhibition of GABA receptors leads to mental confusion, seizures and status epilepticus seen with star fruit intoxication. In this mini-review, we discuss the mechanisms of star fruit-related toxicity.
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PMID:Mechanisms of star fruit (Averrhoa carambola) toxicity: A mini-review. 3296 29