Linked Life Data

3375817

Source:http://linkedlifedata.com/resource/pubmed/id/3375817

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4857
pubmed:dateCreated
1988-7-5
pubmed:abstractText
The present study was undertaken to examine the possibility that cerebral energy metabolism can be fueled by lactate. As a sole energy substrate, lactate supported normal synaptic function in rat hippocampal slices for hours without any sign of deterioration. Slices that were synaptically silent as a result of glucose depletion could be reactivated with lactate to show normal synaptic function. When slices were exposed to the glycolytic inhibitor iodoacetic acid, lactate-supported synaptic function was unaffected, whereas that supported by glucose was completely abolished. This indicated that lactate was metabolized directly via pyruvate to enter the tricarboxylic acid cycle. Thus, under conditions that lead to lactate accumulation (cerebral ischemia) this "end product" may be a useful alternative as a substrate for energy metabolism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
240
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1326-8
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Lactate-supported synaptic function in the rat hippocampal slice preparation.
pubmed:affiliation
Department of Anesthesiology, University of Louisville School of Medicine, KY 40292.
pubmed:publicationType
Journal Article, Comparative Study