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Role of Glutamate Transporters in the Clearance and Release of Glutamate during Ischemia and its Relation to Neuronal Death

Camacho, Alberto, Massieu, Lourdes·2006·Archives of Medical Research
DOI 10.1016/j.arcmed.2005.05.014
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Abstract

Glutamate neurotransmitter action on postsynaptic receptors is terminated by its clearance from the synaptic cleft by transporter proteins located in neurons and glial cells. Failure of glutamate removal can lead to neuronal death due to its well-known neurotoxic properties. Glutamate transporters are dependent on external Na+, and thus on the activity of Na+/K+ ATPases, which maintain the Na+ concentration gradient. When the energy brain requirements are not fulfilled by the appropriate blood supply of glucose and oxygen, the Na+ gradient collapses leading to impaired glutamate and aspartate removal, or even to the release of these amino acids through the reverse operation of their transporters. Such a scenario would be associated with brain ischemia and hypoglycemia due to the prompt decline in ATP levels. In addition, some evidence suggests that downregulation of glutamate transporters after the ischemic period, or the dysfunction induced by oxidation, contributes to the accumulation of extracellular glutamate and neuronal death. Neuronal damage is associated with excitotoxicity, a type of cell death triggered by the overactivation of glutamate receptors and the loss of calcium homeostasis. Throughout this review we will discuss recent evidence suggesting that failure of glutamate transport during ischemia contributes to the elevation of extracellular glutamate and to the induction of excitotoxicity. We will also discuss the contribution of glial vs. neuronal glutamate tra…

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Metadata

Authors
Camacho, A., & Massieu, L.
Venue
Archives of Medical Research
Publisher
Elsevier BV
Published
2006-01
Volume
37
Issue
1
Pages
11-18
ISSN
0188-4409
DOI
10.1016/j.arcmed.2005.05.014
Cited by
150
References
1
Language
en
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