[Cerebral hypoxic and ischemic damage in newborn infants: cellular mechanisms and role of excitatory amino acids].
Brain damage from hypoxia-ischemia plays a major role in neonatal mortality and morbidity. Different lesional mechanisms have been proposed. The most recent hypothesis involves the excitatory amino acids, especially glutamate. In this review, arguments in favour of a glutamate involvement in the lesional process are presented, with particular attention to the consequences of glutamate fixation on post synaptic receptors, especially N-methyl-D-aspartate receptors. Alterations of the intracellular concentration of calcium may also play a role in the pathogenesis of hypoxic-ischemic lesions. A better understanding of the metabolic processes could lead to new therapeutic possibilities.
Cortey
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Service de médecine et réanimation néonatales, maternité régionale universitaire, Nancy, France.
D000818:Animals; D002545:Brain Ischemia / Q000150:complications* / Q000378:metabolism* / Q000628:therapy; D002118:Calcium / Q000032:analysis; D018846:Excitatory Amino Acids / Q000378:metabolism*; D005971:Glutamates / Q000633:toxicity; D006801:Humans; D002534:Hypoxia, Brain / Q000150:complications* / Q000378:metabolism* / Q000628:therapy; D007231:Infant, Newborn; D017470:Receptors, Glutamate / Q000378:metabolism; D009435:Synaptic Transmission
D018846:Excitatory Amino Acids; D005971:Glutamates; D017470:Receptors, Glutamate; D002118:Calcium
Lésions cérébrales hypoxiques et ischémiques du nouveau-né: mécanismes cellulaires et participation des acides aminés excitateurs.