Objective The aim of this work was to ascertain whether the memory disturbance following scopolamine administration and the neuroprotective effect of could be evidenced in global cerebral ischemia by evaluating improved cognitive capacity in the rats. Materials and Methods Neuronal cell density was measured by counting viable cells in the left and right CA1 regions of three coronal sections of 30 um. Behavior test; Acquisition deficits after ischemia.. Use passive avoidance test. Results Neuroprotective effect of GB at 100mg/kg is 87.3%. Representative photomicrographs of cresyl violet-stained hippocampal regions of either sham-operated animals(A,B) or animals that had been subjected to 10 min ischemia followed by the treatment with either saline (C,D) or 100mg/kg of Ginkgo biloba (E,F). Boxed regions in A, C, and E are shown in B, D, and F, respectively. The 10 min ischemia caused selective and delayed neuronal cell loss in the hippocampal CA1 region (C,D). In contrast, GB treatment conferred neuroprotection by markedly reducing the number of damaged pyramidal cells in the CA1 subfield (E,F). Scale bar is 100 um. Effect of GB on scopolamine induced memory deficits in the passive avoidance test. At 30 min after trainining trials, scopolamine(1mg/kg i.p.) or the same volume of saline was administered to rats. At 30 min after scopolamine injection, the rats were treated with GB(100mg/kg). Acquisition trials were carried out 30 min after GB treatment. At 24 hr after acquisition trials, the test trials were carried out. Data represents mean ± SEM (n=6).