Linked Life Data

17459717

Source:http://linkedlifedata.com/resource/pubmed/id/17459717

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-5-22
pubmed:abstractText
Severe hypoglycemia constitutes a medical emergency, involving seizures, coma and death. We hypothesized that seizures, during limited substrate availability, aggravate hypoglycemia-induced brain damage. Using immature isolated, intact hippocampi and frontal neocortical blocks subjected to low glucose perfusion, we characterized hypoglycemic (neuroglycopenic) seizures in vitro during transient hypoglycemia and their effects on synaptic transmission and glycogen content. Hippocampal hypoglycemic seizures were always followed by an irreversible reduction (>60% loss) in synaptic transmission and were occasionally accompanied by spreading depression-like events. Hypoglycemic seizures occurred more frequently with decreasing "hypoglycemic" extracellular glucose concentrations. In contrast, no hypoglycemic seizures were generated in the neocortex during transient hypoglycemia, and the reduction of synaptic transmission was reversible (<60% loss). Hypoglycemic seizures in the hippocampus were abolished by NMDA and non-NMDA antagonists. The anticonvulsant, midazolam, but neither phenytoin nor valproate, also abolished hypoglycemic seizures. Non-glycolytic, oxidative substrates attenuated, but did not abolish, hypoglycemic seizure activity and were unable to support synaptic transmission, even in the presence of the adenosine (A1) antagonist, DPCPX. Complete prevention of hypoglycemic seizures always led to the maintenance of synaptic transmission. A quantitative glycogen assay demonstrated that hypoglycemic seizures, in vitro, during hypoglycemia deplete hippocampal glycogen. These data suggest that suppressing seizures during hypoglycemia may decrease subsequent neuronal damage and dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0969-9961
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
646-60
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17459717-Action Potentials, pubmed-meshheading:17459717-Adenosine A1 Receptor Antagonists, pubmed-meshheading:17459717-Animals, pubmed-meshheading:17459717-Anticonvulsants, pubmed-meshheading:17459717-Cortical Spreading Depression, pubmed-meshheading:17459717-Disease Models, Animal, pubmed-meshheading:17459717-Excitatory Amino Acid Antagonists, pubmed-meshheading:17459717-Glucose, pubmed-meshheading:17459717-Glycogen, pubmed-meshheading:17459717-Hippocampus, pubmed-meshheading:17459717-Hypoglycemia, pubmed-meshheading:17459717-Male, pubmed-meshheading:17459717-Mice, pubmed-meshheading:17459717-Mice, Inbred C57BL, pubmed-meshheading:17459717-Midazolam, pubmed-meshheading:17459717-Nerve Degeneration, pubmed-meshheading:17459717-Neurons, pubmed-meshheading:17459717-Receptor, Adenosine A1, pubmed-meshheading:17459717-Seizures, pubmed-meshheading:17459717-Synaptic Transmission
pubmed:year
2007
pubmed:articleTitle
Hypoglycemic seizures during transient hypoglycemia exacerbate hippocampal dysfunction.
pubmed:affiliation
Division of Fundamental Neurobiology, Toronto Western Research Institute, University Health Network MCL12-413, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario, 416-603-5040, Canada M5T2S8.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't