Abstract
Glutamate is an important: excitatory aminoacid neurotransmitter that mediates neuronal death. Dopamine has also ben implicated, an endugenous substance in the pathogenesis of H-I brain damage. We studied the effects of perinatal H-I insult 1-2A hours after recirculation on glutamate release and dopamine (D1) binding sites in piglet brain (4-7d) (HPLC and (3H)SCH23390 respectively). Transient cerebral ischemia was induced by bilateral carotid occlusion, hypoxia by 8 %. oxgyen, 9 2 %, nitrogen for 10 min. 6 piglets served as normal-control (S-C) 6 as sham-operated (S-O); and 6 as (H-I). Experimental injury result in a significant increase in glutamic acid and glutamine in two vulnerable areas : striatum (stri) and hyppocampus (hip). There was no significant alteration in D1 receptors.
The results suggest that transient cerebral H-I can cause, important release of glutamat, at an early stage of recirculation, and that Dopamine DI transmission is not responsible for the evolution of H-I brain damage. The reduction in DI receptors reproted 7-21d after H-I insult are rather a reflection of cell loss induced by the injury.
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Saliba, E., Chalon, S. & Laugier, J. EFFECT OF HYPOXIC-ISCHEMIC (H-I) BRAIN DAMAGE ON GLUTAMATE RELEASE AND Dl MARKERS IN THE NEWBORN PIGLET. Pediatr Res 35, 281 (1994). https://doi.org/10.1203/00006450-199402000-00161
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DOI: https://doi.org/10.1203/00006450-199402000-00161