M. Gottlieb et al., Altered expression of the glutamate transporter EAAC1 in neurons and immature oligodendrocytes after transient forebrain ischemia, J CEREBR B, 20(4), 2000, pp. 678-687
Glutamate uptake is reduced during ischemia because of perturbations of ion
ic gradients across neuronal and glial membranes. Using immunohistochemical
and Western blot analyses, the authors examined the expression of the glut
amate transporters EAAC1, GLAST, and GLT-1 in the rat hippocampus and cereb
ral cortex 8 hours and 1 to 28 days after transient forebrain ischemia. Den
sitometric analysis of immunoblots of CA1 homogenates showed a moderate inc
rease in EAAC1 protein levels early after the insult. Consistently, it was
observed that EAAC1 immunostaining in CA1 pyramidal neurons was more intens
e after 8 hours and 1 day of reperfusion and reduced at later postischemia
stages. A similar transient increase of EAAC1 immunolabeling was detected i
n layer V pyramidal neurons of the cerebral cortex. In addition, the author
s observed that EAAC1 also was located in oligodendroglial progenitor cells
in subcortical white matter. The number of EAAC1-labeled cells in this reg
ion was increased after 3 and 28 days of reperfusion. Finally, changes in G
LAST and GLT-1 expression were not observed in the CA1 region after ischemi
a using immunohistochemical study or immunoblotting. Enhanced expression of
EAAC1 may be an adaptive response to increased levels of extracellular glu
tamate during ischemia.