Actions of ATP on the soma of bullfrog primary afferent neurons and its modulating action on the GABA-induced response.

Adenosine 5'-triphosphate (ATP) produced a long-lasting depolarization in bullfrog spinal ganglion cells. Since the ATP-induced slow depolarization was associated with an increase in membrane resistance and a reverse in polarity (about--90 mV) which was most likely brought about by an inactivation of membrane potassium conductance. In some cells, a rapid and transient depolarization followed by the long-lasting depolarization was produced by ATP and it was markedly reduced in sodium-free solution. ATP reversibly augmented the GABA-induced depolarization which was caused by ionophoresis of GABA. These observations were confirmed using a voltage clamp method. Dose-response analysis of the action of ATP on the GABA-induced response suggests that the facilitatory action of ATP on the GABA response is effected on the GABA receptor channel complexes without changing the GABA affinity.