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.