Profiling neuroendocrine gene expression changes following fadrozole-induced estrogen decline in the female goldfish.

Abstract:

:Teleost fish represent unique models to study the role of neuroestrogens because of the extremely high activity of brain aromatase (AroB; the product of cyp19a1b). Aromatase respectively converts androstenedione and testosterone to estrone and 17beta-estradiol (E2). Specific inhibition of aromatase activity by fadrozole has been shown to impair estrogen production and influence neuroendocrine and reproductive functions in fish, amphibians, and rodents. However, very few studies have identified the global transcriptomic response to fadrozole-induced decline of estrogens in a physiological context. In our study, sexually mature prespawning female goldfish were exposed to fadrozole (50 mcirog/l) in March and April when goldfish have the highest AroB activity and maximal gonadal size. Fadrozole treatment significantly decreased serum E2 levels (4.7 times lower; P = 0.027) and depressed AroB mRNA expression threefold in both the telencephalon (P = 0.021) and the hypothalamus (P = 0.006). Microarray expression profiling of the telencephalon identified 98 differentially expressed genes after fadrozole treatment (q value <0.05). Some of these genes have shown previously to be estrogen responsive in either fish or other species, including rat, mouse, and human. Gene ontology analysis together with functional annotations revealed several regulatory themes for physiological estrogen action in fish brain that include the regulation of calcium signaling pathway and autoregulation of estrogen receptor action. Real-time PCR verified microarray data for decreased (activin-betaA) or increased (calmodulin, ornithine decarboxylase 1) mRNA expression. These data have implications for our understanding of estrogen actions in the adult vertebrate brain.

journal_name

Physiol Genomics

journal_title

Physiological genomics

authors

Zhang D,Popesku JT,Martyniuk CJ,Xiong H,Duarte-Guterman P,Yao L,Xia X,Trudeau VL

doi

10.1152/physiolgenomics.00051.2009

subject

Has Abstract

pub_date

2009-08-07 00:00:00

pages

351-61

issue

3

eissn

1094-8341

issn

1531-2267

pii

00051.2009

journal_volume

38

pub_type

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