The effects of hydrostatic pressure on signal transduction in brain membranes of deep-sea fishes of the genus Coryphaenoides
To investigate the effects of increased hydrostatic pressure on transmembrane signaling in deep-living marine species, the A1 adenosine receptor - inhibitory G protein (Gi) - adenylyl cyclase signaling complex was examined in brain membrane preparations from four teleost fish species of the deep-sea family Macrouridae. The combined depth ranges of the adults of these species, Coryphaenoides armatus, C. cinereus, C. filifer, C. pectoralis, span several hundred meters to 5400 m. Basal adenylyl cyclase activity, determined at 5 °C, was inhibited by increased hydrostatic pressure in all four species. At the highest pressure tested, 476 atm, adenylyl cyclase activity was inhibited 60 to 70% relative to the atmospheric pressure values. Pressure inhibition did not result from denaturation or loss of protein components from the membrane due to pressure-induced shedding. Despite the pressure-inhibition of basal adenylyl cyclase activity, the responsiveness of adenylyl cyclase activity to modulation by N6-cyclopentyladenosine, an A1 adenosine receptor agonist, was retained at elevated pressures. Because the accumulation of the second messenger cAMP depends on the summation of modulatory inputs, these results indicate that the transmembrane signaling in these deep-living species is insensitive to hydrostatic pressure changes.