Hk. Lu et al., CA2-DEPENDENT ACTIVATION OF T-TYPE CA2+ CHANNELS BY CALMODULIN-DEPENDENT PROTEIN-KINASE-II(), The American journal of physiology, 267(1), 1994, pp. 60000183-60000189
The T-type Ca2+ channel is unique among voltage-dependent Ca2+ channel
s in its low threshold for opening and its slow kinetics of deactivati
on. Here, we evaluate the importance of intracellular Ca2+ (Ca-i(2+))
in promoting low-threshold gating of T-type channels in adrenal glomer
ulosa cells. We observe that 390 nM to 1.27 mu M Ca-i(2+) enhances T-t
ype current by shifting the voltage dependence of channel activation t
o more negative potentials. This Ca2+-induced shift is mediated by cal
modulin-dependent protein kinase II (CaMKII), because it is abolished
by inhibitors of CaMKII but not of protein kinase C and is subsequentl
y restored by exogenous calmodulin. This Ca2+-induced reduction in gat
ing threshold would render T-type Ca2+ channels uniquely suited to tra
nsduce depolarizing stimuli of low amplitude into a Ca2+ signal suffic
ient to support a physiological response.