Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1987-1-22
|
| pubmed:abstractText |
Here I have reviewed evidence from electron microscopic studies showing that each of several sustained limbic seizure syndromes is associated with a type of acute brain damage which is ultrastructurally indistinguishable from the brain damage induced by Glu and other excitotoxins. In addition, I have presented evidence that persistent stimulation of specific axonal tracts that use Glu as transmitter results in Glu-like excitotoxic degeneration of postsynaptic neurons innervated by such tracts. Phencyclidine and ketamine, which powerfully block the neurotoxicity of the Glu analog NMA, protect against seizure-related brain damage. This may be explained by either an anticonvulsant or antiexcitotoxic mechanism, or both. Recent evidence suggests that an excitotoxic mechanism (excessive activation of Glu/Asp receptors) may underlie both seizure-mediated and anoxic brain damage. The acute fulminating type of neuronal degeneration induced by Glu is a Na+ and Cl- but not Ca2+ dependent phenomenon. According to a recent study, however, Glu may induce neuronal necrosis not only by an acute Ca2+ independent process but by a more slowly evolving Ca2+ dependent process. If, as these data suggest, an excitotoxic mechanism underlies brain damage associated with anoxia and epilepsy, a better understanding of excitotoxic mechanisms may lead eventually to prophylactic approaches for preventing such forms of brain damage.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Folic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Ketamine,
http://linkedlifedata.com/resource/pubmed/chemical/Parasympathomimetics,
http://linkedlifedata.com/resource/pubmed/chemical/Phencyclidine,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/dipiperidinoethane
|
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0065-2598
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
203
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
631-45
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:3024464-Action Potentials,
pubmed-meshheading:3024464-Animals,
pubmed-meshheading:3024464-Anoxia,
pubmed-meshheading:3024464-Brain,
pubmed-meshheading:3024464-Cell Survival,
pubmed-meshheading:3024464-Chick Embryo,
pubmed-meshheading:3024464-Cholinergic Fibers,
pubmed-meshheading:3024464-Disease Models, Animal,
pubmed-meshheading:3024464-Edema,
pubmed-meshheading:3024464-Epilepsies, Partial,
pubmed-meshheading:3024464-Folic Acid,
pubmed-meshheading:3024464-Hippocampus,
pubmed-meshheading:3024464-Kainic Acid,
pubmed-meshheading:3024464-Ketamine,
pubmed-meshheading:3024464-Microscopy, Electron,
pubmed-meshheading:3024464-Parasympathomimetics,
pubmed-meshheading:3024464-Phencyclidine,
pubmed-meshheading:3024464-Piperidines,
pubmed-meshheading:3024464-Seizures,
pubmed-meshheading:3024464-Synaptic Transmission,
pubmed-meshheading:3024464-Thalamus
|
| pubmed:year |
1986
|
| pubmed:articleTitle |
Inciting excitotoxic cytocide among central neurons.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|