2006
Neuronal–Glial Glucose Oxidation and Glutamatergic–GABAergic Function
Hyder F, Patel AB, Gjedde A, Rothman DL, Behar KL, Shulman RG. Neuronal–Glial Glucose Oxidation and Glutamatergic–GABAergic Function. Cerebrovascular And Brain Metabolism Reviews 2006, 26: 865-877. PMID: 16407855, DOI: 10.1038/sj.jcbfm.9600263.Peer-Reviewed Original ResearchConceptsGamma-amino butyric acid (GABA) neuronsNeuronal glucose oxidationGlutamate-glutamine cyclingRelease of lactateGlucose oxidationNeuronal oxidationGlial uptakeGABAergic neuronsGlutamate uptakeGliaNeuronsGlycolytic ATPLactateGlucoseTotal glucoseVivo rateIsoelectricityCulture studiesATPNeurotransmittersUptake
2001
Decrease in GABA synthesis rate in rat cortex following GABA-transaminase inhibition correlates with the decrease in GAD67 protein
Mason G, Martin D, Martin S, Manor D, Sibson N, Patel A, Rothman D, Behar K. Decrease in GABA synthesis rate in rat cortex following GABA-transaminase inhibition correlates with the decrease in GAD67 protein. Brain Research 2001, 914: 81-91. PMID: 11578600, DOI: 10.1016/s0006-8993(01)02778-0.Peer-Reviewed Original ResearchConceptsTotal GAD activityGAD activityNon-treated control groupGABA-transaminase inhibitionNitrous oxide anesthesiaCortex of controlGlutamate-glutamine cyclingGlutamic acid decarboxylaseGABA synthesis rateGamma-aminobutyric acid (GABA) synthesisVigabatrin treatmentOxide anesthesiaRat cortexGAD67 proteinControl groupBasal conditionsAcid decarboxylaseEx vivoNeuronal compartmentsVigabatrinQuantitative immunoblottingIsoform compositionRatsCortexInhibition