Transmitter amino acid release from rat neocortex: complete versus incomplete ischemia models.
Release of the excitotoxic amino acids, glutamate and aspartate, from the ischemic rat cerebral cortex was compared in two models; the seven vessel occlusion model (7VO) of complete cerebral ischemia and the four vessel occlusion model (4VO) of incomplete cerebral ischemia. Amino acid efflux into cortical superfusates was measured using cortical cups placed on both hemispheres. Whereas a 20 min period of ischemia causes a pronounced release of glutamate and aspartate from the 4VO model, efflux was significantly reduced in the 7VO model. Release of the inhibitory transmitter GABA, was similar in the two models. This result suggests that excitotoxic amino acid efflux into the extracellular spaces of the cerebral cortex may be enhanced by the residual blood flow in an incomplete ischemia.
Phillis
J W
JW
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201.
Perkins
L M
LM
Smith-Barbour
M
M
O'Regan
M H
MH
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001794:Blood Pressure; D002540:Cerebral Cortex / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D005110:Extracellular Space / Q000378:metabolism; D007839:Functional Laterality; D018698:Glutamic Acid / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D015424:Reperfusion; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid