test_moissonnage_selune
type: Agent

Effect of vitamin A status on glucocorticoid pathway and consequences on memory processes in rodents
type: Distribution
access URL: https://theses.hal.science/tel-00957462
format: HTML
issued: 2026-05-06T02:23:17.984704
modified: 2026-05-06T02:23:17.953078

Effect of vitamin A status on glucocorticoid pathway and consequences on memory processes in rodents
type: Dataset
contact point: Organization
  fn: CCSD
keyword: neurogenese
keyword: carence-en-vitamine-a
keyword: hippocampe
keyword: glucocorticoids
keyword: aging
keyword: hippocampus
keyword: vitamin-a-deficiency
keyword: neurogenesis
keyword: glucocorticoides
keyword: cerebral-plasticity
keyword: supplementation-en-vitamine-a
keyword: acide-retinoique
keyword: retinoic-acid
keyword: sdvotlife-sciences-q-bioother-q-bioot
keyword: memoire
keyword: vitamin-a-supplementation
keyword: theses
keyword: memory
keyword: plasticite-synaptique
keyword: infoeu-reposemanticsdoctoralthesis
keyword: vieillissement
landing page: https://theses.hal.science/tel-00957462
description: It is now established that vitamin A and its active metabolite, retinoic acid (RA), are required for cognitive functions in the adult hood. The hyposignaling of retinoic acid and the hyperactivity of the glucocorticoid (GC) pathway appear concomitantly during aging and both would contribute to the deterioration of hippocampal plasticity and functions. Moreover, recent data have evidenced counteracting effects of retinoids on the GC signaling pathway.The goal of the present study has been to shed more light on the interactions between both signaling pathways and their consequences on cerebral plasticity and memory processes.We have investigated them not only in a well-established nutritional model of vitamin A deficiency but also during aging. Indeed, our experimental approach has consisted inmanipulating the status in vitamin A (deficiency and/or supplementation or RA treatment) inrodents to better understand its impact on plasma and intrahippocampal corticosterone levelsand the mechanisms involved in corticosterone bioavailability. Hippocampus-dependentmemory and plasticity (adult neurogenesis and synaptic plasticity-related gene expression)have also been assessed.We have shown a hyperactivity of the glucocorticoid pathway in vitamin A-deficientrats, leading to elevated peripheral and hippocampal corticosterone levels. This is probably due to a decrease in CBG binding capacity and to the hyperactivity of the hippocampal 11β-HSD1. Furthermore, a vitamin A supplementation normalizes glucocorticoid activity and hippocampal neurogenesis levels and corrects memory deficits.Besides, in middle-aged mice, a RA treatment is able to positively modulate the retinoidsignaling pathway inducing a decreased hypersecretion of intrahippocampal corticosterone. It thus counteracts the deleterious effects of an excess of glucocorticoids on neurobiological and memory processes.Altogether, these results contribute to the demonstration that in vitamin A deficiency and during aging, the s…
identifier: NNT: 2013BOR14977
issued: 2026-05-06T02:23:17.976338
language: fr
modified: 2026-05-06T02:23:17.976343