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Abstract
Recent studies have revealed a novel and unexpected role of vitamin A, via its nuclear receptors, in higher cognitive functions. We examined, in mouse brain, the impact of vitamin A status on the level of retinoic acid nuclear receptor (RAR and RXR) expression and on one of their responsive genes, that of the tissue transglutaminase (tTG). Weanling male C57B1/6 mice fed a vitamin A deficient diet developed a vitamin A deficiency which was characterized, after 26 weeks, by the depletion of serum retinol, liver retinol and retinyl palmitate, and by the decreased activity of liver tTG. After 27 weeks of the diet, the vitamin A depleted mice exhibited a significantly lower amount of brain RAR β and RXR β/γ mRNA relative to control mice. Vitamin A deficiency also resulted in a reduced expression of tTG. When 35-week depleted mice were subsequently administrated RA for 28 days, the expression of RA nuclear receptors and tTG was significantly induced. The vitamin A deficiency mouse model and repletion provides a physiological system for monitoring the effects of vitamin A status on gene expression and on neurobiological processes in the adult brain.