Temperature modulates the Ca2+ current of HIT-T15 and mouse pancreatic beta-cells.

The effects of raising temperature on the Ca2+ currents of insulin-secreting 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 increased peak Ca2+ current amplitude, percent (fast) inactivation and decreased the time-to-peak of the current. Ca2+ currents in HIT and mouse beta-cells responded in the same manner to an imposed physiological burstwave with test-pulses: (i) application of the burstwave inactivated the test-pulse Ca2+ current at both high and low temperatures; (ii) Ca2+ current inactivation leveled off during the plateau phase at 20-22 degrees C whereas there was an apparent continual decay at 33-35 degrees C; and (iii) recovery from inactivation occurred during the interburst period at both temperatures. Application of a physiological burstwave without test-pulses to mouse beta-cells before and after addition of 0.2 mM Cd2+ resulted in a Ca2+ difference current. This current activated during the hyperpolarized interburst phase, activated, inactivated and deactivated rapidly and continually during the plateau phase, and recovered from inactivation during the interburst. Although raising temperature strongly modified HIT and mouse beta-cells Ca2+ current, our work suggests that other channels, in addition to Ca2+ channels, are likely to be involved in the control of islet bursts, particularly at different temperatures. In addition, the effect of temperature on islet cell Ca2+ current may be partly responsible for the well-known temperature dependence of glucose-dependent secretion.