Early regulation of brain aromatase (cyp19a1b) by estrogen receptors during zebrafish development

Developmental expression of genes involved in neural estrogen biosynthesis and signaling in the brain of the orange-spotted grouper Epinephelus coioides during gonadal sex differentiation

“…This finding was confirmed in several teleost fishes including the Atlantic salmon, Salmo salar [19], stickleback (Gasterosteus aculeatus) [20], African catfish (Clarias gariepinus) [21], European sea bass (Dicentrarchus labrax) [16] and peacock blenny (Salaria pavo) [22]. This high neural aromatase activity has been attributed to the high levels of neurogenesis present in the teleosts brain compared to mammals [7,13,15]. Moreover, estrogen is an important neurotrophic factor, playing this role throughout life and influencing neuronal differentiation [23,24], participating in the process of embryonic and adult neurogenesis [25,26].…”

“…The quality and concentration of RNA were assessed by spectrophotometry and checked by running an aliquot (1 g) on a 1.8% agarose-formaldehyde gel. The cDNAs were synthesized from 1 g of total RNA using Superscript II (Invitrogen; Carlsbad, CA) and oligo (dT) [12][13][14][15][16][17][18] primers in a 20 l reaction volume with incubation at 42 • C for 60 min, 37 • C for 15 min, and 70 • C for 15 min and cDNAs were then stored at −80 • C until use.…”

“…Brain sex steroids, especially E2, may cause brain sex differentiation at an early developmental age and lead to sexually dimorphic adult reproductive behaviors in mammals [8,9]. In addition, aromatase activity is regulated by estrogens and aromatizable androgens, and several studies in teleost fish indicate that cyp19a1b transcripts are up-regulated by E2 through estrogen receptor signaling [10][11][12][13], indicating the reproductive role and functional relationship of estrogen with brain aromatase. However, another study indicated that the cyp19a1b gene is also up-regulated by androgens, especially T, suggesting a potential androgenic regulation of cyp19a1b through the estrogen receptor [14].…”

Low-dose exposure to bisphenol A and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish

“…Furthermore, we propose that we have uncovered a temporal competency window for BPA effects on hypothalamic neurogenesis that is separate from estrogen signaling. This phenotype could be caused by changes in the expression of all three zebrafish ERs (ERα, ERβ1, and ERβ2), which increases dramatically between 24 and 48 hpf (53). Given that the peak of BPA susceptibility occurs at 24 hpf, and we show a role for ARs in BPA-mediated precocious neurogenesis, it will be interesting to see whether AR expression increases earlier than ER expression in the developing hypothalamus.…”

“…For example, proliferating cells in the developing cortex, hippocampus, olfactory bulb, and hypothalamus all express ERs (48) and ARs (25,49), and a clear role for sex steroids (e.g., estrogen, testosterone) in regulating neurogenesis in vivo (26,28) and in vitro (50, 51) is emerging, especially in the adult brain (27,29,52). In embryonic and adult zebrafish, ERs and AroB are coexpressed in hypothalamic radial glia and are thought to control differentiation and migrational changes that occur in response to estrogen exposure (29,53). These findings have led to the notion that AroB-expressing radial glia are plastic and initiate adult neurogenesis in response to estrogenic challenges as a way to maintain homeostatic physiologies (52).…”