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In vivo neuroprotective adaptation of the glutamate/glutamine cycle to neuronal death

✍ Scribed by D. Ramonet; M.J. Rodríguez; K. Fredriksson; F. Bernal; N. Mahy

Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
523 KB
Volume
14
Category
Article
ISSN
1050-9631

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✦ Synopsis

Abstract

Synaptic increase of glutamate level, when not coupled to a heightened energy production, renders neurons susceptible to death. Astrocyte uptake and recycling of synaptic glutamate as glutamine is a major metabolic pathway dependent on energy metabolism, which interrelationships are not fully understood and remain controversial. We examine how the glutamate‐glutamine cycle and glucose metabolism are modified in two in vivo models of severe and mild brain injury. Graded reductions of glutaminase, the glutamate synthetic enzyme, were evidenced combined with increases in glutamine synthetase, the inactivating glutamate enzyme. Increased lactate dhydrogenase (LDH) activity was only present after a more severe injury. These results indicate an in vivo adaptation of the glutamate‐glutamine cycle in order to increase the net glutamine output, reduce glutamate excitotoxicity, and avoid neuronal death. We conclude that the graded modification of the glutamate‐glutamine correlation and neuronal lactate availability may be key factors in the apoptotic and necrotic neuronal demise, whose control may prove highly useful to potentiate neuronal survival. © 2004 Wiley‐Liss, Inc.

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