CorrectionsNEUROBIOLOGY. For the article ''Remodeling of ␣-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit composition in hippocampal neurons after global ischemia'' by Thoralf Optiz, Sonja Y. Grooms, Michael V. L. Bennett, and R. Suzanne Zukin, which appeared in number 24, November 21, 2000, of Proc. Natl. Acad. Sci. USA (97,(13360)(13361)(13362)(13363)(13364)(13365), the authors note the following correction. The name of the first author was misspelled. The correct spelling is Thoralf Opitz. The online version has been corrected. In control vector-treated wells, KA significantly increased ROS accumulation (P Ͻ 0.05 and 0.01 in GT and Bcl-2 studies, respectively, post hoc test after two-way ANOVA). In GT-infected wells, KA did not significantly increase accumulation, and in either condition (ϮKA), there was significantly less accumulation than in cognate control wells (P Ͻ 0.01 for both). In contrast, KA significantly increased accumulation in Bcl-2-treated wells (P Ͻ 0.05), and values did not differ significantly from the cognate control wells. (B) Effects of GT or Bcl-2 on metabolism in primary hippocampal cultures under hypoglycemic conditions as assessed by proton efflux rates, measured by microphysiometry. vIE1GT (Left) attenuated the drop of metabolism posthypoglycemia ( *** , P Ͻ 0.001 by post hoc test after two-way ANOVA, comparing experimental vector versus control vector at the same time point), whereas v␣22␤gal␣4bcl-2 (Right) had no effect. Data on the Left previously published (7), making use of a related HSV vector expressing either GT (vIE1GT) or ␤-Gal as a reporter gene (vIE1␤Gal). excitotoxicity ͉ neuronal death ͉ excitatory amino acid ͉ glutamate ͉ calcium