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Previous investigations in mice have shown that vitamin A deficiency (VAD) generates a hypo-expression of retinoic acid (RA, the active metabolite of vitamin A) receptors and of neurogranin (RC3, a neuronal protein involved in synaptic plasticity) and a concomitant selective behavioural impairment. Knowing that RC3 is both a triiodothyronine (T<jats:sub>3<\/jats:sub>) and a RA target gene, and in consideration of the relationships between the signalling pathways of retinoids and thyroid hormones, the involvement of T<jats:sub>3<\/jats:sub>on RA signalling functionality in VAD was investigated. Thus, the effects of vitamin A depletion and subsequent administration with RA and\/or T<jats:sub>3<\/jats:sub>on the expression of RA nuclear receptors (RAR, RXR), T<jats:sub>3<\/jats:sub>nuclear receptor (TR) and on RC3 in the brain were examined. Rats fed a vitamin A-deficient diet for 10 weeks exhibited a decreased expression of RAR, RXR and TR mRNA and of RC3 mRNA and proteins. RA administration to these vitamin A-deficient rats reversed only the RA hypo-signalling in the brain. Interestingly, T<jats:sub>3<\/jats:sub>is able to restore its own brain signalling simultaneously with that of vitamin A and the hypo-expression of RC3. These results obtained in vivo revealed that one of the consequences of VAD is a dysfunction in the thyroid signalling pathway in the brain. This seems of crucial importance since the down regulation of RC3 observed in the depleted rats was corrected only by T<jats:sub>3<\/jats:sub>.<\/jats:p>","DOI":"10.1079\/bjn2003877","type":"journal-article","created":{"date-parts":[[2003,7,9]],"date-time":"2003-07-09T21:42:52Z","timestamp":1057786972000},"page":"191-198","source":"Crossref","is-referenced-by-count":39,"title":["Triiodothyronine administration reverses vitamin A deficiency-related hypo-expression of retinoic acid and triiodothyronine nuclear receptors and of neurogranin in rat 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