TY  - JOUR
A1  - Boese, Stefan H.
A1  - Gray, Michael A.
A1  - Simmons, N. L.
T1  - Volume and non-volume activated anion conductances and their interactions in the renal IMCD
Y1  - 2004
SN  - 0-387- 23299-0
ER  - 
TY  - JOUR
A1  - Sayer, J. A.
A1  - Stewart, G. S.
A1  - Boese, Stefan H.
A1  - Gray, Michael A.
A1  - Pearce, S. H. S.
A1  - Goodship, T. H. J.
A1  - Simmons, N. L.
T1  - A voltage-dependent Cl- channel, CLC-5 and plasma membrane Cl- conductances of mouse renal collecting duct cells (mlMCD-3)
Y1  - 2001
SN  - 0022-3751
ER  - 
TY  - JOUR
A1  - Linley, John E.
A1  - Boese, Stefan H.
A1  - Simmons, Nicholas L.
A1  - Gray, Michael A.
T1  - A voltage-dependent Ca2+ influx pathway regulates the Ca2+-dependent Cl- conductance of renal IMCD-3 cells
N2  - We have previously shown that the membrane conductance of mIMCD-3 cells at a holding potential of 0 mV is dominated by a Ca2+-dependent Cl- current (I-CLCA). Here we report that I-CLCA activity is also voltage dependent and that this dependence on voltage is linked to the opening of a novel Al3+-sensitive, voltage-dependent, Ca2+ influx pathway. Using whole-cell patch-clamp recordings at a physiological holding potential (-60 mV), I-CLCA was found to be inactive and resting currents were predominantly K+ selective. However, membrane depolarization to 0 mV resulted in a slow, sigmoidal, activation of I-CLCA (T (0.5) similar to 500 s), while repolarization in turn resulted in a monoexponential decay in I-CLCA (T (0.5) similar to 100 s). The activation of I-CLCA by depolarization was reduced by lowering extracellular Ca2+ and completely inhibited by buffering cytosolic Ca2+ with EGTA, suggesting a role for Ca2+ influx in the activation of I-CLCA. However, raising bulk cytosolic Ca2+ at -60 mV did not produce sustained I-CLCA activity. Therefore I-CLCA is dependent on both an increase in intracellular Ca2+ and depolarization to be active. We further show that membrane depolarization is coupled to opening of a Ca2+ influx pathway that displays equal permeability to Ca2+ and Ba2+ ions and that is blocked by extracellular Al3+ and La3+. Furthermore, Al3+ completely and reversibly inhibited depolarization-induced activation of I-CLCA, thereby directly linking Ca2+ influx to activation of I-CLCA. We speculate that during sustained membrane depolarization, calcium influx activates I-CLCA which functions to modulate NaCl transport across the apical membrane of IMCD cells.
Y1  - 2009
UR  - http://www.springerlink.com/content/100360
U6  - https://doi.org/10.1007/s00232-009-9186-0
SN  - 0022-2631
ER  -