TEMPERATURE MODULATES THE CA2-T15 AND MOUSE PANCREATIC BETA-CELLS( CURRENT OF HIT)

The effects of raising temperature on the Ca2+ currents of insulin-sec reting HIT and mouse pancreatic beta-cells were studied. Currents were measured in 3 mM Ca2+ containing solutions using standard whole-cell techniques. Increasing temperature from 22 degrees C to 35 degrees C i ncreased peak Ca2+ current amplitude, percent (fast) inactivation and decreased the time-to-peak of the current. Ca2+ currents in HIT and mo use beta-cells responded in the same manner to an imposed physiologica l burstwave with test-pulses: (i) application of the burstwave inactiv ated the test-pulse Ca2+ current at both high and low temperatures; (i i) Ca2+ current inactivation leveled off during the plateau phase at 2 0-22 degrees C whereas there was an apparent continual decay at 33-35 degrees C; and (iii) recovery from inactivation occurred during the in terburst period at both temperatures. Application of a physiological b urstwave without test-pulses to mouse beta-cells before and after addi tion of 0.2 mM Cd2+ resulted in a Ca2+ difference current. This curren t activated during the hyperpolarized interburst phase, activated, ina ctivated and deactivated rapidly and continually during the plateau ph ase, and recovered from inactivation during the interburst. Although r aising temperature strongly modified HIT and mouse beta-cell Ca2+ curr ent, our work suggests that other channels, in addition to Ca2+ channe ls, are likely to be involved in the control of islet bursts, particul arly at different temperatures. In addition, the effect of temperature on islet cell Ca2+ current may be partly responsible for the well-kno wn temperature dependence of glucose-dependent secretion.