GLUCOSE ATTENUATION OF ATROPINE-INDUCED DEFICITS IN PARADOXICAL SLEEPAND MEMORY

When administered systemically, glucose attenuates deficits in memory produced by several classes of drugs, including cholinergic antagonist s and opiate agonists. Glucose also enhances memory in aged rats, mice , and humans. In addition, glucose ameliorates age-related reductions in paradoxical sleep. Because deficits in paradoxical sleep are most m arked in those individual aged rats that also have deficits in memory, treatments which improve one of these functions may similarly improve the other. The present experiments show that glucose attenuates defic its in paradoxical sleep and memory after atropine administration, wit h similar dose-response curves for both actions. In the first experime nt, rats received saline, atropine (1 mg/kg), glucose (100 mg/kg) or c ombinations of atropine + glucose (10, 100, 250, and 500 mg/kg) 30 min before assessment on a spontaneous alternation task. In the second ex periment, 3-h EEGs were assessed far spontaneous daytime sleep in rats administered saline, atropine (1 mg/kg), glucose (100 mg/kg) or combi nations of atropine + glucose (10, 100 and 250 mg/kg). In both experim ents, glucose significantly attenuated deficits at an optimal dose of 100 mg/kg. A third experiment assessed blood glucose levels after inje ctions of atropine + glucose (100 mg/kg) and determined that blood glu cose levels were similar to those produced by other treatments which e nhance memory. These results are consistent with the view that paradox ical sleep and at least one test of memory are similarly influenced by atropine and glucose.