Modified K-channel gating by exhaustion and the block by internally applied TEA+ and 4-aminopyridine in muscle

Abstract

Voltage clamp experiments on frog sartorius muscle fibres suggest that the large increase in resting potassium conductance during metabolic exhaustion is due to a change in the gating of activated potassium channels to a permanently open state. g_K in exhausted fibres is less sensitive to externally applied blockers as Zn²⁺ and 4-aminopyridine (4-AP) while TEA⁺, Rb⁺ and Ba²⁺ act similarly, both in normal and exhausted fibres. In addition, injection experiments provide evidence that TEA⁺ and 4-AP applied internally to normal fibres effectively block potassium outward current, whereas in exhausted fibres the block seems to be smaller. These results suggest modifications in the structure of the potassium channels during metabolic exhaustion.