Chemically induced K+ conduction noise in squid axon.
Internal perfusion of tetraethylammonium ions (TEA) in squid axons produces a significant high frequency noise component. Although internal TEA suppresses the potassium conductance (GK) noise at relatively low frequencies, it induces high frequency noise which exceeds the intensity of the normal potassium and sodium noise. In addition, the induced noise is dependent on the presence of internal potassium ions (K+) suggesting that this source of noise arises from a modulation of the K+ conductance due to the blocking and unblocking of the K+ channel. The simplest model describing the TEA data is a two-step sequential, pseudo-unimolecular reaction where TEA binds during an open conductance state. A unit channel conductance of 2 pS is estimated from the TEA data as well as noise induced by triethyldecylammonium (TEDA) ions. Thus, these data are consistent with the hypothesis that the channel is blocked whenever the quaternary ammonium ion binding site, located near or within the K+ channel, is occupied.
D000818:Animals; D001369:Axons / Q000502:physiology*; D001665:Binding Sites; D002462:Cell Membrane / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects; D049832:Decapodiformes; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism*; D013757:Tetraethylammonium Compounds / Q000378:metabolism / Q000494:pharmacology*
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D011188:Potassium