Glucose attenuation of deficits in memory retrieval in altered light:dark cycles

Previous studies in rats show that disrupting circadian light-dark rhythms leads to impairments in memory. In particular, both phase delays and phase advances of the light:dark cycle initiated after inhibitory (passive) avoidance training result in impaired retention. The present study examined this phenomenon in mice and, using a retrieval design, examined whether glucose or epinephrine could attenuate deficits in memory. Groups of mice were first trained on an inhibitory avoidance task during the light portion of the illumination cycle. They were then maintained for a 72-h train-test interval either under the same schedule of illumination or one with a phase advance of 4 h. Thirty minutes before testing, groups were injected with saline, glucose (1, 10, 100, 250, or 500 mg/kg), or epinephrine (0.1 mg/kg). The results showed that (1) retention was significantly impaired in phase-shifted mice relative to nonphase-shifted controls and (2) both glucose (100 mg/kg) and epinephrine attenuated the deficit in memory. These findings indicate that altered illumination schedules disrupt memory in mice as well as in rats. In addition, they suggest that glucose may be a useful treatment to attenuate deficits in memory associated with impaired biological rhythms.