This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pascual, J. M. Articles by Koehler, R. C. Search for Related Content PubMed PubMed Citation Articles by Pascual, J. M. Articles by Koehler, R. C.

(Stroke. 1998;29:1048-1057.)
© 1998 American Heart Association, Inc.

Original Contributions

Glutamate, Glutamine, and GABA as Substrates for the Neuronal and Glial Compartments After Focal Cerebral Ischemia in Rats

José M. Pascual, MD; Fernando Carceller, MD, PhD; José M. Roda, MD, PhD; Sebastián Cerdán, PhD

From the Servicio de Neurocirugía, Hospital La Paz (J.M.P., F.C., J.M.R.), and Instituto de Investigaciones Biomédicas del C.S.I.C. (S.C.), Madrid, Spain.

Correspondence to Dr Sebastian Cerdán, Instituto de Investigaciones Biomédicas del C.S.I.C., c/Arturo Duperier 4, E-28029 Madrid, Spain. E-mail scerdan{at}biomed.iib.uam.es

Background and Purpose—Even though the utilization of substrates alternative to glucose may play an important role in the survival of brain cells under ischemic conditions, evidence on changes in substrate selection by the adult brain in vivo during ischemic episodes remains very limited. This study investigates the utilization of glutamate, glutamine, and GABA as fuel by the neuronal and glial tricarboxylic acid cycles of both cerebral hemispheres after partially reversible focal cerebral ischemia (FCI).

Methods—Right hemisphere infarct was induced in adult Long-Evans rats by permanent occlusion of the right middle cerebral artery and transitory occlusion of both common carotid arteries. (1,2-¹³C₂) acetate was infused for 60 minutes in the right carotid artery immediately after carotid recirculation had been re-established (1-hour group) or 23 hours later (24-hour group). Extracts from both cerebral hemispheres were prepared and analyzed separately by ¹³C nuclear magnetic resonance and computer-assisted metabolic modeling.

Results—FCI decreased the oxidative metabolism of glucose in the brain in a time-dependent manner. Reduced glucose oxidation was compensated for by increased oxidations of (¹³C) glutamate and (¹³C) GABA in the astrocytes of the ipsilateral hemispheres of both groups. Increased oxidative metabolism of (¹³C) glutamine in the neurons was favored by increased activity of the neuronal pyruvate recycling system in the 24–hour group.

Conclusions—Data were obtained consistent with time-dependent changes in the utilization of glutamate and GABA or glutamine as metabolic substrates for the glial or neuronal compartments of rat brain after FCI.

Editorial Comment

Raymond C. Koehler, PhD, Guest Editor

Anesthesiology/Critical Care Medicine The Johns Hopkins University Baltimore, Maryland

This article has been cited by other articles:

				J. P. van der Zijden, P. van Eijsden, R. A. de Graaf, and R. M. Dijkhuizen 1H/13C MR spectroscopic imaging of regionally specific metabolic alterations after experimental stroke Brain, August 1, 2008; 131(8): 2209 - 2219. [Abstract] [Full Text] [PDF]

				S. S. Zoghbi, H. U. Shetty, M. Ichise, M. Fujita, M. Imaizumi, J.-S. Liow, J. Shah, J. L. Musachio, V. W. Pike, and R. B. Innis PET Imaging of the Dopamine Transporter with 18F-FECNT: A Polar Radiometabolite Confounds Brain Radioligand Measurements J. Nucl. Med., March 1, 2006; 47(3): 520 - 527. [Abstract] [Full Text] [PDF]

				K. L. Behar and D. L. Rothman In Vivo Nuclear Magnetic Resonance Studies of Glutamate-{gamma}-Aminobutyric Acid-Glutamine Cycling in Rodent and Human Cortex: the Central Role of Glutamine J. Nutr., September 1, 2001; 131(9): 2498S - 2504. [Abstract] [Full Text] [PDF]

				L. Hertz, S. R. Robinson;, J. L. Griffin;, P. J. Magistretti, L. Pellerin, R. G. Shulman, and D. L. Rothman; Energy for Neurotransmission Science, July 30, 1999; 285(5428): 639a - 639. [Full Text]