Cloned neuronal IK(A) channels reopen during recovery from inactivation.
The kinetic behaviour and functional role of potassium ion (K+) channels mediating a fast-inactivating K+ current (IK(A)) has been widely discussed. Activating in the subthreshold range of excitation, IK(A) channels are assumed to reduce the excitatory effect of depolarizing membrane currents in a time-dependent manner. Here we report that IK(A) channels not only open in response to a depolarization but open again after repolarization of the membrane. Although the current in response to the depolarization is rapidly inactivating, the current elicited by repolarization declines slowly and produces long-lasting afterhyperpolarizations under current-clamp conditions. This implies an additional physiological role for IK(A) channels, particularly those that activate positive to the threshold of excitation. The underlying biophysical mechanism was studied by fast-application of peptides corresponding to the N-terminal end of the IK(A) channel proteins. It was found to be a voltage-dependent release of the inactivation gate.
Max-Planck-Institut für Medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.
J P
JP
Ruppersberg
R
R
Frank
O
O
Pongs
M
M
Stocker
D000595:Amino Acid Sequence; D000818:Animals; D003001:Cloning, Molecular; D004330:Drosophila; D004553:Electric Conductivity; D015640:Ion Channel Gating / Q000502:physiology*; D008564:Membrane Potentials; D008969:Molecular Sequence Data; D010446:Peptide Fragments / Q000737:chemistry / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*
D010446:Peptide Fragments; D015221:Potassium Channels; D011188:Potassium