Proposed model of ion channel targets through which NO results in a prolonged depolarization.
Elevation of NO by NO donors, such as NOC7 or DEA/NO, inhibits two types of Ca2+-activated K+ channels in Helisoma B19 neurons. Apamin-sensitive SK channels contribute to part of the initial effect of NO and are fully responsible for its long-lasting effect on membrane depolarization, whereas IbTX-sensitive BK channels only partially contribute to the initial depolarization. Voltage-gated Ca2+ channels do not participate in the depolarizing effect of extrinsically applied NO. The mechanism(s) by which NO inhibits these ion channels is presently unknown (indicated by dotted lines). Inhibitors used are indicated in gray.