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.
D000255:Adenosine Triphosphate / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005727:Ganglia, Spinal / Q000187:drug effects*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects; D011892:Rana catesbeiana; D005680:gamma-Aminobutyric Acid / Q000008:administration & dosage*
D007473:Ion Channels; D005680:gamma-Aminobutyric Acid; D000255:Adenosine Triphosphate