Glucose injections attenuate deficits in memory under several conditions in both rodents and humans. The present study examined effects of glucose on memory in two such amnesic populations, scopolamine-treated and old mice, and then assessed effects of glucose on brain [3H]2-deoxyglucose (2DG) uptake. In Experiment 1A, scopolamine (3 mg/kg, i.p.) significantly impaired performance of mice tested in a spontaneous alternation task. Glucose (100 mg/kg, i.p.) administration did not itself affect alternation performance, but when administered with scopolamine, it attenuated the deficit in alternation performance. Scopolamine (3 mg/kg) also resulted in significant reductions in brain 2DG uptake in hippocampus and in thalamus (Experiment 1B). Glucose (100 mg/kg) injections did not themselves affect 2DG uptake, but when administered with scopolamine, they attenuated the scopolamine-induced reductions in 2DG uptake, with the largest reversal occurring in hippocampus. Glucose similarly enhanced spontaneous alternation behavior (Experiment 2A) and hippocampal 2DG uptake (Experiment 2B) in 2-year-old mice. These findings provide additional evidence that the brain becomes more sensitive to circulating glucose in several amnestic conditions and, more generally, extend the view that circulating levels of glucose influence a wide range of brain activities.
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