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Department of Autonomic Physiology, Tokyo Medical and Dental University, Japan.

1. Intracellular recordings were made from myenteric neurones isolated from the guinea-pig small intestine to study actions of adenosine 5'-triphosphate (ATP). ATP was applied by superfusion (10 nM-100 microM) or pressure ejection from ATP-containing glass pipettes. 2. Myenteric neurones have been classified into two groups: type I/S neurones and type II/AH neurones. ATP produced a membrane hyperpolarization in 80% of AH neurones and a membrane depolarization in 90% of S neurones in a dose-dependent manner. Adenosine caused responses similar to those induced by ATP in both AH and S neurones, but was less effective than ATP. 3. The ATP-induced hyperpolarization was associated with a fall in input resistance, but the ATP-induced depolarization was accompanied by an increase in input resistance. Both responses reversed in polarity near the potassium equilibrium potential (-84 to -87 mV) and the reversal potential varied with extracellular potassium concentration, as predicted by the Nernst equation. These results indicate that the hyperpolarization is due to an increase, while the depolarization is due to a decrease in potassium conductance. 4. Both the hyperpolarization and the depolarization induced by ATP persisted in calcium-free solution containing 1.2 mM-magnesium, but were markedly reduced or abolished in calcium-free solutions containing 3.7-10 mM-magnesium and by 1 mM-nickel or cobalt. Both responses to ATP persisted in tetraethylammonium (1-10 mM) or tetrodotoxin (1-3 microM)-containing solutions. 5. Quinine and quinidine (1-100 microM) reversibly depressed both the ATP-induced responses. Caffeine (100 microM), theophylline (100 microM) and 3-isobutyl-1-methylxanthine (1-10 microM) did not significantly affect the ATP-induced depolarization but did reversibly depress the ATP-induced hyperpolarization. 6. These results suggest that the ATP-induced hyperpolarization may be due to activation, and the ATP-induced depolarization to inactivation, of a calcium-sensitive potassium conductance.

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