Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2002-7-5
pubmed:abstractText
The study aimed at determining mechanism(s) by which amobarbital (amytal) suppresses glucose oxidation in cerebellar granule neurons in primary cultures, a glutamatergic preparation. When challenged with a depolarizing K(+) concentration (55 mM), the cells doubled their rate of glucose oxidation (production of 14CO(2) from U-[14C]glucose) and glycolysis (lactate accumulation). At normal K(+) concentration, amobarbital reduced 14CO(2) production with half-maximum effect at 0.5-1 mM; at 55 mM K(+), the inhibition was more potent, with more than half of the K(+)-induced stimulation abolished at 50 microM. Dixon plot analysis showed a single inhibitory mechanism at 5.4 mM K(+), but at 55 mM K(+), two kinetically different mechanisms could be distinguished. A more pronounced compensatory amobarbital-induced increase in glycolysis at 5.4 than at 55 mM K(+) suggested that amobarbital in addition to its inhibition of mitochondrial respiration inhibited K(+)-induced increase in energy demand, probably by its known suppression of stimulated glutamate release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
446
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-61
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Amobarbital inhibits K(+)-stimulated glucose oxidation in cerebellar granule neurons by two mechanisms.
pubmed:affiliation
Hong Kong DNA Chips, Limited, Kowloon, Hong Kong, China.
pubmed:publicationType
Journal Article