Estradiol-17β modulates ER-aromatase and thyroid hormone receptor-regulator (TR-R) gene expression and energy markers in brain segments of stressed female air-breathing fish (Anabas testudineus Bloch).

Estradiol-17β (E2) regulates many physiological processes in fish. E2 and thyroid hormone (TH) interact in fish, but their effects on the stressed fish brain remain poorly understood. We hypothesised that E2 may interact with TH via their receptors and regulators, thereby affecting energy metabolism during stress acclimation in fish brain segments. We thus examined the short-term (60 min) in vivo effect of E2 on the expression patterns of the E2 receptor-aromatase (ER-arom) system, such as erα, erβ, cyp19a1a, cyp19a1b, and the thyroid hormone receptor and regulator (TR-R) system, such as trα, trβ, trαb, deo1, deo2, deo3, mct8, mct10, as well as energy provision in the brain segments of female air-breathing fish (Anabas testudineus) held under net-confined (NC) stress conditions. NC stress activated all these transcripts across the brain segments, most prominently in the mesencephalon (MC) segment. E2 selectively modulated ER-arom and TR-R transcript expression across brain segments of NC-stressed fish. The Venn diagram analysis showed that E2 enhanced several receptor gene transcripts (erβ, cyp19a1b, trα, trβ, trαb) and attenuated regulatory (Deo) or transport (Mct) genes in MC segments. Furthermore, E2 shifted energy metabolism towards anaerobic pathways in the stressed MC segment, as indicated by a reversal of the increase in COX activity and a decrease in LDH activity. These data indicate that E2 plays a crucial role in coordinating ER-arom and TR-R systems under stress, suggesting that E2 may safeguard the fish brain by differentially regulating these systems and reversing high energy demands across brain segments during stress acclimation.