ATP release from the electric organ of Torpedo and from Xenopus oocytes

A field-stimulated electric organ generated an electric field and release o f a large quantity of ATP. Oocytes injected with mRNA from a Torpedo electr ic organ released ATP when stimulated with carbamylcholine. We set up a con figuration recording that let us simultaneously monitor the the oocyte ioni c currents and ATP release from a single oocyte. Hyperpolarization pulses a pplied to Xenopus oocytes induced an inward current and release of ATP inde pendently of the expression of the ClC-0 chloride channel. The current was insensitive to substitution of ions in the extracellular saline solution, e ither anions or cations. The reversal potential of the current was establis hed between +40 and +100 mV, which is in the same range as the equilibrium potential of ATP(-4). There was a correlation between the magnitude of the inward current and the all-count of MP released. The inward current closed slowly. During this closing period there was still release of ATP, which is sensitive to the holding potential, Positive potentials cut the amount of ATP released. The evoked current and ATP release were both sensitive to inh ibitors of E-NTPDase activity such as suramin, 4-acetamido-4'isothiocyanato stilbene-2,2'-disulfonic acid (SITS), 4,4'diisothiocyanatostilbene-2'-disul fonic acid (DIDS), and a high concentration of calcium and gadolinium ions. The expression of CD39 increased the size of the hyperpolarizing induced c urrent. By reverse transcription polymerase chain reaction, we found a prot ein homologous to CD39. The relationship between the results obtained in th e electric organ and oocytes is that, in both cases, stimulation or hyperpo larization causes a change in the intracellular ion concentration, producin g an osmotic stress, which, in turn, triggers ATP release. Stimulation or h yperpolarization may alter the intercellular ion concentration, leading to osmotic stress and the release of ATP in both electric organ and oocytes. D rug Dev. Res. 52:34-43, 2001. (C) 2001 Wiley-Liss, Inc.