In Vivo Action of Nitric Oxide Donor Sodium Nitroprusside (SNP) on Mitochondrial Ion Transporter Function in Brain Segments of Immersion-Stressed Air-Breathing Fish ( Anabas testudineus Bloch)

Abstract

The neuronal circuitries of brain and the corresponding ion transporters contribute to the maintenance of ion homeostasis in fish brain. The sensitivity of these neuronal clusters in response to environmental clues brings neural plasticity and subsequent regulation of stress acclimation. Nitric oxide (NO), a gasotransmitter, is involved in ion transport in many peripheral tissues of fishes including air-breathing fish. However, the role of NO in mitochondrial ion transporter activity has not yet been investigated in fish brain. We, therefore, investigated the short-term in vivo action of a NO donor, Sodium Nitro-Prusside (SNP), on mitochondrial ion transporters such as H + - Ca 2+ - and Mg 2+ -dependent ATPases in brain segments such as Prosen-Cephalon (PC), Mesen-Cephalon (MC) and Meten-Cephalon (MeC) of immersion-stressed Anabas testudineus . Intraperitoneal injection of SNP for 30 min lowered the activities of bafilomycin-sensitive H + ATPase and vanadate sensitive Ca 2+ ATPase in PC, whereas in MeC, these transporters showed significant rise in activities after SNP treatment. The oligomycin-sensitive Mg 2+ ATPase activity showed a significant decrease in PC and MC of brain after SNP treatment in non-stressed fish. Induction of stress by water immersion altered the activities of these ion transporter activities. However, the treatment of SNP in immersed fish showed recovery of the immersion-induced modulation in the activities of these mitochondrial ion transporters. Our data, thus, provide evidence for a decisive role of NO in the recovery process of mitochondrial ion transporters function during immersion stress, confirming a direct differential role of NO in mitochondrial ion homeostasis in teleost brain.