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Drug–ionic channel interactions: Single‐channel measurements

Ionic channels of excitable membranes are the basic site where ionic fluxes take place during the generation of action potentials. A variety of natural toxins, chemicals, and therapeutic drugs have been found to modify the gating kinetics of the Na+ channels, thereby altering the excitation pattern. Studies of such chemical modulations of Na+ channel gating provide the basis for understanding the mechanisms underlying the epilepsies and the actions of anticonvulsant drugs. Certain chemicals and toxins have been found to drastically slow the kinetics of the opening and closing of the Na+ channel. For example, batrachotoxin, the grayanotoxins, and the pyrethroids modify a population of the Na+ channels to give rise to an extremly slow opening and closing. Patch clamp techniques developed during the past few years permit measurements of the opening and closing of individual ionic channels. When an isolated membrane patch is depolarized, squared inward currents of about 1 picoampere in amplitude and 2 ms in duration are observed at 10°C. After exposure of the membrane to batrachotoxin, open time is prolonged, single‐current amplitude is greatly reduced, and channel opening is observed at large negative potentials, where no opening is expected to occur in normal preparations. In the batrachotoxin‐poisoned membrane there are two separate groups of Na+ channels: one exhibiting normal characteristics and the other exhibiting a prolonged opening and reduced amplitude.