Abstract

Being the principal estrogen, estradiol 17I² (E 2 ) is essential for normal ovarian function in the vertebrates including fishes. Besides its primary role in reproduction, E 2 is also known for its role in many other physiological processes including water and mineral balance. However, it is uncertain, how E 2Â regulates ion-specific ATPases that drive Na + , K + , H + , Ca 2+ and Mg 2+ transport in fish brain. We, therefore, examined the short-term in situ action of E 2 on ion transporter function in the brain segments of freshwater female Mozambique tilapia Oreochromis mossambicus . Tilapia were perfused with increasing doses of E 2 (10 -9 , 10 -8 and 10 -7 M) for 20 min and sampled for determining Na + /K + -ATPase, H + -ATPase, Ca 2+ -ATPase, and Mg 2+ -ATPase activities in the prosencephalon (PC), mesencephalon (MC) and metencephalon (MeC) segments of brain. Dose-dependent increase in Na + /K + - and Ca 2+ -dependent transporter activities after E 2 perfusion were found in PC. In MC, E 2 treatment, however, produced significant increase in Mg 2+ , Ca 2+ and H + transport activities in mitochondria but decreased Na + /K + - and I½H + transporter activities. On the contrary, in MeC, E 2 administration while producing increase in Na + /K + -, mitochondrial- and I½H + -transport, lowered cytosolic and mitochondrial Ca 2+ transport. Taken together, the data indicate that E 2 has rapid and direct action on ion transporter function that corresponds to the differential activation/inactivation of neuronal clusters in the brain segments of female freshwater tilapia.

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