Fig. 7. The effects of InsP₃ receptor blockade on the ability of carbachol (CCh) to suppress STOCs. Depolarisation to -20 mV from a holding potential of -70 mV (iv) induced STOCs (ii) and increased [Ca²⁺]_i (iii). (A) 2-APB (50 µM), a membrane-permeable InsP₃ receptor inhibitor, introduced by perfusion, inhibited the ability of InsP₃ and CCh to affect STOCs (ii and i expanded time base). (i) represents some 30 second excerpts from ii as indicated by the dotted lines. The increased perfusion per se temporarily increased STOC amplitude and was unrelated to the presence of a particular drug. (B) Heparin (2.5 mg/ml), a membrane-impermeable InsP₃ receptor inhibitor, introduced via the patch pipette, was present throughout the entire experiment. Other experiments (not shown) under identical conditions with no heparin present served as controls. In the presence of heparin, neither InsP₃ () nor CCh (10 mM, v) significantly altered the amplitude or frequency (ii and expanded time base i) of STOCs. CCh activated a transient inward current causing the resting level of membrane current to fall (ii).

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