GAD1 and brain ischemia: We assumed that contralateral hippocampal GABAergic and glutamatergic systems-related proteins GAD67 (glutamic acid decarboxylase-67), GA1B (GABAB receptor 1), and NR2B (N-methyl-D-aspartate receptor 2B) were upregulated by EE to further reveal the effects and mechanisms by which EE can improve cognitive function after cerebral ischemia [9–11].