Table of Contents
ISRN Pharmacology
Volume 2012 (2012), Article ID 295853, 8 pages
Research Article

Anticonvulsant Drugs, Brain Glutamate Dehydrogenase Activity and Oxygen Consumption

1Neurochemistry Laboratory, Department of Biochemistry, National School of Biological Sciences, National Polytechnic Institute, Carpio Y Plan de Ayala S/No., Col. Casco de Santo Tomás, 11340 México, DF, Mexico
2Superior School of Medicine, National Polytechnic Institute, Plan de San Luis y Díaz Mirón S/No., Col. Casco de Santo Tomás, 11340 México, DF, Mexico

Received 17 November 2011; Accepted 18 December 2011

Academic Editor: T. W. Stone

Copyright © 2012 Lourdes A. Vega Rasgado et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Glutamate dehydrogenase (GDH, E.C. is a key enzyme for the biosynthesis and modulation of glutamate (GLU) metabolism and an indirect γ-aminobutyric acid (GABA) source, here we studied the effect of anticonvulsants such as pyridoxal phosphate (PPAL), aminooxyacetic acid (AAOA), and hydroxylamine (OHAMINE) on GDH activity in mouse brain. Moreover, since GLU is a glucogenic molecule and anoxia is a primary cause of convulsions, we explore the effect of these drugs on oxygen consumption. Experiments were performed in vitro as well as in vivo for both oxidative deamination of GLU and reductive amination of α-ketoglutarate (αK). Results in vitro showed that PPAL decreased oxidative deamination of GLU and oxygen consumption, whereas AAOA and OHAMINE inhibited GDH activity competitively and also inhibited oxygen consumption when αK reductive amination was carried out. In contrast, results showed that in vivo, all anticonvulsants enhanced GLU utilization by GDH and also decreased oxygen consumption. Together, results suggest that GDH activity has repercussions on oxygen consumption, which may indicate that the enzyme activity is highly regulated by energy requirements for metabolic activity. Besides, GDH may participate in regulation of GLU and, indirectly GABA levels, hence in neuronal excitability, becoming a key enzyme in seizures mechanism.