The Influence of Temperature On the Effects of Acetylcholine and Adrenaline On the Membrane-potential and Rb-86 Efflux in Mouse Pancreatic B-cells

Pancreatic mouse islets were used to evaluate the influence of temperature on the B-cell response to acetylcholine and adrenaline. At 20-degrees-C, the rate of Rb-86 efflux from islet cells was lower, the membrane potential of B-cells was slightly less negative, and glucose-induced electrical activity was characterized by longer slow waves than at 37-degrees-C. At 20-degrees-C, the acceleration of Rb-86 efflux produced by 1-mu-M-ACh was only reduced by 25%, but its reversibility was slower. Acetylcholine rapidly depolarized the B-cell membrane and increased electrical activity regardless of the temperature. However, this increase was characterized by the appearance of short slow waves of high frequency at 37-degrees-C and by continuous spiking at 20-degrees-C. Adrenaline (1-mu-M) inhibited Rb-86 efflux at 37 and 20-degrees-C, but the amplitude of the inhibition was decreased and its time course and reversibility were altered at the lower temperature. Adrenaline repolarized the B-cell membrane and abolished glucose-induced electrical activity for a longer period at 20-degrees-C than at 37-degrees-C. In conclusion, no marked decrease in signal transduction occurs at 20-degrees-C. This suggests that the difficulty of identifying the currents induced by acetylcholine and adrenaline in patch-clamp experiments performed at room temperature is probably due to the small magnitude of these currents.