Journal
AGING CELL
Volume -, Issue -, Pages -Publisher
WILEY
DOI: 10.1111/acel.13928
Keywords
aging; behavioral tests; glycogen phosphorylase (Pyg); hippocampus; memory formation; deficits
Categories
Ask authors/readers for more resources
Inhibition of glycogen breakdown improves memory formation in old mice by stimulating neuroplasticity and affecting hippocampal proteome. However, in young animals, inhibition of glycogen degradation impairs memory formation without significant effects on cortical dendritic spines.
Inhibition of glycogen breakdown blocks memory formation in young animals, but it stimulates the maintenance of the long-term potentiation, a cellular mechanism of memory formation, in hippocampal slices of old animals. Here, we report that a 2-week treatment with glycogen phosphorylase inhibitor BAY U6751 alleviated memory deficits and stimulated neuroplasticity in old mice. Using the 2-Novel Object Recognition and Novel Object Location tests, we discovered that the prolonged intraperitoneal administration of BAY U6751 improved memory formation in old mice. This was accompanied by changes in morphology of dendritic spines in hippocampal neurons, and by rejuvenation of hippocampal proteome. In contrast, in young animals, inhibition of glycogen degradation impaired memory formation; however, as in old mice, it did not alter significantly the morphology and density of cortical dendritic spines. Our findings provide evidence that prolonged inhibition of glycogen phosphorolysis improves memory formation of old animals. This could lead to the development of new strategies for treatment of age-related memory deficits.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available