{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T02:14:44Z","timestamp":1792289684956,"version":"4.4.0"},"reference-count":44,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2002,11,1]],"date-time":"2002-11-01T00:00:00Z","timestamp":1036108800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2002,11]]},"abstract":"\n The effect of deep barbiturate anesthesia on brain glucose transport, TCA cycle flux, and aspartate, glutamate, and glutamine metabolism was assessed in the rat brain in vivo using\n 13<\/jats:sup>\n C nuclear magnetic resonance spectroscopy at 9.4 T in conjunction with [1-\n 13<\/jats:sup>\n C] glucose infusions. Brain glucose concentrations were elevated, consistent with a twofold reduced cerebral metabolic rate for glucose (CMR\n glc<\/jats:sub>\n ) compared with light \u03b1-chloralose anesthesia. Using a mathematical model of neurotransmitter metabolism, several metabolic reaction rates were extracted from the rate of label incorporation. Total oxidative glucose metabolism, CMR\n glc(ox)<\/jats:sub>\n , was 0.33 \u00b1 0.03 \u03bcmol\u00b7g\n \u22121<\/jats:sup>\n \u00b7 min\n \u22121<\/jats:sup>\n . The neuronal TCA cycle rate was similar to that in the glia, 0.35 \u00b1 0.03 \u03bcmol \u00b7 g\n \u22121<\/jats:sup>\n \u00b7 min\n \u22121<\/jats:sup>\n and 0.26 \u00b1 0.06 \u03bcmol \u00b7 g\n \u22121<\/jats:sup>\n \u00b7 min\n \u22121<\/jats:sup>\n , respectively, suggesting that neuronal energy metabolism was mainly affected. The rate of pyruvate carboxylation was 0.03 \u00b1 0.01 \u03bcmol\u00b7g\n \u22121<\/jats:sup>\n \u00b7 min\n \u22121<\/jats:sup>\n . The exchange rate between cytosolic glutamate and mitochondrial 2-oxoglutarate, V\n x<\/jats:sub>\n , was equal to the rate of neuronal pyruvate dehydrogenase flux. This indicates that V\n x<\/jats:sub>\n is coupled to CMR\n glc(ox)<\/jats:sub>\n , implying that the malate-aspartate shuttle is the major mechanism that facilitates label exchange across the inner mitochondrial membrane. The apparent rate of glutamatergic neurotransmission, V\n NT<\/jats:sub>\n , was 0.04 \u00b1 0.01 \u03bcmol\u00b7g\n \u22121<\/jats:sup>\n \u00b7 min\n \u22121<\/jats:sup>\n , consistent with strong reductions in electrical activity. However, the rates of cerebral oxidative glucose metabolism and glutamatergic neurotransmission, CMR\n glc(ox)<\/jats:sub>\n \/V\n NT<\/jats:sub>\n , did not correlate with a 1:1 stoichiometry.\n <\/jats:p>","DOI":"10.1097\/01.wcb.0000040945.89393.46","type":"journal-article","created":{"date-parts":[[2015,12,15]],"date-time":"2015-12-15T13:09:09Z","timestamp":1450184949000},"page":"1343-1351","source":"Crossref","is-referenced-by-count":98,"title":["Effect of Deep Pentobarbital Anesthesia on Neurotransmitter Metabolism\n in Vivo<\/i>\n : On the Correlation of Total Glucose Consumption with Glutamatergic Action"],"prefix":"10.1177","volume":"22","author":[{"given":"In-Young","family":"Choi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongxia","family":"Lei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rolf","family":"Gruetter","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, University of Minnesota, Center for MR Research, Minneapolis, Minnesota, 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