Glucose attenuation of scopolamine- and age-induced deficits in spontaneous alternation behavior and regional brain [3H]2-deoxyglucose uptake in mice

Abstract

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 (lHJ2deoxyglucose (2DG) uptake. In Experiment lA, 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 lB). 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.Acute peripheral administration of glucose near the time of training enhances memory in rodents and humans (

Glucose attenuation of memory impairments.

“…This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. is consistent with the findings of Stone et al (1992), who found that 100 mg/kg glucose ameliorated a large scopolamine impairment in spontaneous alternation, to a level of performance no different from that of a saline control. Figure 3 shows mean discriminability (logaf) measures plotted as a function of retention interval for each dose level of glucose for Birds B4 and B5.…”

“…The present finding-that administration of dose levels of glucose up to 100 mg/kg did not improve matching accuracy or discriminability above that of vehicle control-is consistent with previous findings in which glucose by itself did not enhance short-term memory performance in either DMTS (Ahlers et al, 1993) or spontaneous alternation (Stone et al, 1992) procedures. When taken in the context of other findings in which glucose was effective in enhancing performance in aversive tasks, such as the aversive one-trial inhibitory (passive) avoidance task (Stone et al, 1990), it may be concluded that the enhancing effects of glucose are evident only when the short-term memory task involves aversive events.…”

“…A separate session conducted with a lower dose level of scopolamine (0.02 mg/kg) for these 2 pigeons produced an average reduction in proportion correct from 0.81 to 0.56. This reduction in matching accuracy as a result of scopolamine administration is consistent with the results of several studies with pigeons (Ruske et al, 1997;Teal & Evans, 1982) and other species (Bartus, 1978;Blanchard & Duncan, 1997;Stone et al, 1992).…”

“…Stone, Rudd, and Gold (1990) administered glucose to mice 30 min before retention tests on an aversive inhibitory (passive) avoidance task and found that glucose significantly enhanced learning. In contrast, when administered 30 min before a nonaversive spontaneous alternation task (in which performance was related to the ability to remember previous selections), glucose did not by itself affect alternation performance (Stone et al, 1991;Stone, Rudd, & Gold, 1992). In addition, Ahlers, Shurtleff, Schrot, Thomas, and Paul-Emile (1993) administered glucose to rats 1 hr before testing them on a nonaversive delayed matching-to-sample (DMTS) task.…”

Scopolamine- and morphine-induced impairments of spontaneous alternation performance in mice: Reversal with glucose and with cholinergic and adrenergic agonists.

“…Considerable evidence indicates that Cholinergic antagonists impair memory in animals and humans (e.g., Drachman, 1977;Flood & Cherkin, 1986;Spencer, Pontecorvo, & Heise, 1985;Troster, Beatty, Staton, & Rorabaugh, 1989). Recent findings indicate that glucose and epinephrine attenuate amnesia for inhibitory avoidance training produced by the muscarinic antagonist scopolamine (Stone, Croul, & Gold, 1988). Introini-Collison and McGaugh (1988) also reported substantial interactions between epinephrine and Cholinergic agents; in that study, epinephrine potentiated the memory-enhancing effects of the Cholinergic agonists oxotremorine and physostigmine but did not reverse atropine-induced amnesia.…”