Enhanced brain expression of genes related to cell proliferation and neural differentiation is associated with cortisol receptor expression in fishes
|Author(s)||Sadoul Bastien1, Alfonso Sebastien1, 2, Bessa E.3, Bouchareb A.4, Blondeau-Bidet E.6, Clair P.5, Chatain Beatrice1, Begout Marie-Laure2, Geffroy Benjamin1|
|Affiliation(s)||1 : Univ Montpellier, MARBEC, Ifremer, CNRS,IRD, Palavas Les Flots, France.
2 : Ifremer, Lab Ressources Halieut La Rochelle, Pl Gaby Coll, Lhoumeau, France.
3 : Univ Brasilia, Grad Program Ecol, Brasilia, DF, Brazil.
4 : Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
5 : Univ Montpellier, Montpellier GenomiX, Montpellier, France.
|Source||General And Comparative Endocrinology (0016-6480) (Academic Press Inc Elsevier Science), 2018-10 , Vol. 267 , P. 76-81|
|WOS© Times Cited||3|
|Keyword(s)||Neurogenesis, Stress, Glucocorticoid receptor, Mineralocorticoid receptor, Hypothalamo-pituitary-interrenal axis|
Stress enhances or inhibits neurogenesis in mammals and some fish species. The link between the two processes is still unclear. Most studies have been performed in very specific stressful or altered environments. Despite the known inter-individual divergence in coping abilities within populations, the relationship between the stress axis and neurogenesis has never been addressed in unstressed individuals. Here we correlate brain expression of the pcna (proliferating cell nuclear antigen) and neurod1 (neurogenic differentiation factor 1) genes, two markers of neurogenesis, with transcripts of cortisol receptors in three fish species living in very distinct environments. Within the three species, individuals with the highest expression of neurogenesis genes were also those that expressed the high levels of cortisol receptors. Based on these correlations and the hypothesis that mRNA levels are proxies of protein levels, we hypothesize that within unstressed animals, individuals sensitive to cortisol perceive a similar environment to be more stimulating, leading to increased neurogenesis. Although it is difficult to determine whether it is sensitivity to cortisol that affects neurogenesis capacities or the opposite, the proposed pathway is a potentially fruitful avenue that warrants further mechanistic experiments.