Modified K-channel gating by exhaustion and the block by internally applied TEA+ and 4-aminopyridine in muscle.
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. gK 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.
D000818:Animals; D001001:Anura; D005221:Fatigue / Q000378:metabolism*; D008564:Membrane Potentials; D009132:Muscles / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011725:Pyridines / Q000494:pharmacology*; D011896:Rana temporaria; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*
D011725:Pyridines; D013757:Tetraethylammonium Compounds; D011188:Potassium