Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation

Abstract

Ample research indicates that age-related neuronal-behavioral decrements are the result of oxidative stress that may be ameliorated by antioxidants. Our previous study had shown that rats given dietary supplements of fruit and vegetable extracts with high antioxidant activity for 8 months beginning at 6 months of age retarded age-related declines in neuronal and cognitive function. The present study showed that such supplements (strawberry, spinach, or blueberry at 14.8, 9.1, or 18.6 gm of dried aqueous extract per kilogram of diet, respectively) fed for 8 weeks to 19-month-old Fischer 344 rats were also effective in reversing age-related deficits in several neuronal and behavioral parameters including: oxotremorine enhancement of K(+)-evoked release of dopamine from striatal slices, carbachol-stimulated GTPase activity, striatal Ca(45) buffering in striatal synaptosomes, motor behavioral performance on the rod walking and accelerod tasks, and Morris water maze performance. These findings suggest that, in addition to their known beneficial effects on cancer and heart disease, phytochemicals present in antioxidant-rich foods may be beneficial in reversing the course of neuronal and behavioral aging.

Figures

Fig. 1.

Oxotremorine enhancement of DA release (A) and differences (expressed as change from baseline) in carbachol-stimulated low KM GTPase activity (B) from striatal slices obtained and prepared from animals maintained on the control or the various antioxidant diets (mean + SEM). Means not sharing a common letter are significantly different from each other (p < 0.05; Fisher’s LSD).

Fig. 2.

Calcium recovery (A; expressed as percent of control) and increase in calcium (B; expressed as percent increase) in synaptosomes obtained from animals in the various diet groups and exposed to 0 or 300 μmH2O2 (15 min) and depolarized with 60 mm KCl. For this figure, a differs from untreated (no H2O2) control diet group,b differs from treated (H2O2) control diet group, and theasterisk indicates a difference between 0 and 300 μm H2O2 for that diet group (p < 0.05; Fisher’s LSD).

Fig. 3.

Performance (latency to fall, in seconds) on the rod walk (A) and rotarod (B) tests for the various diet groups. Means not sharing a common letter are significantly different from each other (p < 0.05; Fisher’s LSD).

Fig. 4.

Morris water maze performance in the various diet groups. Performance was assessed over 4 d (2 sessions per day, 2 trials per session). Results are given as latencies (A) and distances (B) to find the hidden platform for the first and second trials for each session on days 3 and 4. Asterisks indicate a difference between trial 1 and trial 2 performance for that diet group (*p < 0.05; **p < 0.01; ***p < 0.001; Fisher’s LSD).

Fig. 5.

DCF fluorescence in the striata (expressed as percent of control) in the various diet groups (A). Means not sharing a common letter are statistically different from each other (p< 0.05; Fisher’s LSD). B shows total striatal glutathione levels among the four groups.