Postnatal ontogeny of expression of the corticosteroid receptor genes in mammalian brains: inter-species and intra-species differences.
Corticosteroids are important mediators of homeostasis and stress, and exert their effects via two transcription-factor receptors, mineralocorticoid receptor (MR) and glucocorticoid receptor (GR). Both receptors are expressed in the brain in a region-specific manner, and regulate neuroendocrine and behavioral functions. Stress during early development has been demonstrated to lead to long-term alterations in MR and GR levels and in the phenotypes that they mediate. To date, however, nearly all of this evidence has been obtained in rats, and there is actually no clear basis for extrapolation to other species. The current comparative review presents data, as available, on the following aspects of GR and MR gene expression in mouse and rat (Rodentia), tree shrew (Scandentia), common marmoset, squirrel monkey, rhesus macaque and human (Primates): (1) species-typical adult expression of MR mRNA and GR mRNA in hypothalamus, amygdala, hippocampus and neocortex; (2) species-typical neonate, infant, juvenile/adolescent and adult expression of MR mRNA and GR mRNA in hippocampus. (1) and (2) allow for identification of inter-species consistencies and differences in the relative levels of MR and GR expression across brain regions and ontogenetic stages. In addition, data are presented on (3) within-species inter-individual variation in MR and GR expression and causes thereof, including polymorphism and early life stress. Integrating the evidence in (1)-(3), it is noted that, should the expression levels of MR and GR at the time of early-life stress determine the latter's effects on the formers' long-term expression levels and functioning, then the long-term effects of early life stress on corticosteroid receptor expression and function will be species-, brain-region- and receptor-type-specific.
Pryce
Christopher R
CR
Neuroscience/Psychiatry, Novartis Institutes for Biomedical Research, Novartis Pharma AG, Basel, Switzerland. Christopher.pryce@novartis.com
D000818:Animals; D001921:Brain / Q000502:physiology*; D015870:Gene Expression; D006801:Humans; D010828:Physiology, Comparative; D011987:Receptors, Steroid / Q000096:biosynthesis* / Q000235:genetics; D013045:Species Specificity
D011987:Receptors, Steroid