Delayed-rectifier Conductance Research Articles

The Potassium Delayed Rectifier Conductance in the Sarcolemma and the Transverse Tubular System Membranes of Mammalian Skeletal Muscle Fibers

The transverse tubular system (TTS) plays a key role not only in mediating the mechanism of excitation-contraction coupling, but also in determining the electrical properties of mammalian skeletal muscle fibers. We investigated the properties and distribution (between sarcolemma and TTS membranes) of the K delayed rectifier conductance (gKV) by simultaneously recording fluorescence transients and ionic currents (IKV) from FDB muscle fibers stained with the potentiometric indicator di-8-ANEPPS and voltage-clamped using a two-microelectrode configuration. Enzymatically dissociated fibers were mounted on the stage of an inverted fluorescence microscope equipped with a 460-500//500//513-558nm cube. The external solution had (in mM): 150 LiCl, 4 KCl, 20 MOPS, 2 CaCl2, 1MgCl2 and 10 glucose. The Na, ClC-1, Ca and KIR currents were blocked by external TTX (0.001), 9-ACA (0.4), nifedipine (0.02) and Rb (5), respectively. The membrane capacitance was measured after rendering the fibers electrically passive by replacing external Li and K by TEA. We found that IKV records display a delayed onset and decayed markedly during long depolarizing pulses (400ms) due to inactivation and accumulation mechanisms. Furthermore, while di-8-ANNEPS transients recorded from electrically passive fibers displayed quasi-rectangular kinetic properties, transients recorded from control fibers in the presence of IKV were associated with time-dependent attenuations that matched the kinetics of activation and decay of IKV records. Radial cable model simulations were used to evaluate the voltage-dependent kinetic parameters of gKV, to calculate the rate of accumulation of K+ ions in the lumen of the TTS, and to determine that the relative distribution of this conductance between the surface and TTS membranes is close to equal. This work was supported by NIH grants AR047664, AR041802, and AR054816.

K+Channels and Their Modulation by 5-HT in Drosophila Photoreceptors: A Modelling Study

In order to clarify the role of inactivating and noninactivating K+ conductances in nonspiking neurons, we developed an isopotential model of the Drosophila photoreceptor membrane based on Hodgkin-Huxley-type equations. The model includes voltage dependent potassium conductances, the shaker (gKA) and the delayed rectifier (gKs). The model parameters were derived from published results by Hardie and coworkers and nearly identical model was used also in our previous work (J. E. Niven, M. Vähäsöyrinki, M. Kauranen, R. C. Hardie, M. Juusola, and M. Weckström. The Contribution of shaker K+ channels to the information capacity of Drosophila photoreceptors. Nature. 421:630-634, 2003). The model explains how the two types of channels function together to define the voltage dependent properties of the photoreceptor membrane. Additionally the model enables us to run simulations of conditions which are difficult to achieve in patch clamp, like prolonged membrane depolarizations by light adaptation. Effects of the activation of the delayed rectifier type conductance were found to be in accordance with published experimental work but the inactivation of the shaker channels, in addition to its importance in the determination of the resting potential, produced voltage amplification over equivalent passive membrane under dark adapted conditions. This phenomenon was not present in light adapted conditions. The modulation of the voltage dependence of the conductances as reported by serotonin (5-HT) caused the shaker to act essentially like the delayed rectifier conductance.

A delayed rectifier conductance shapes the voltage response of type I hair cells.

Annals of the New York Academy of SciencesVolume 781, Issue 1 p. 690-692 A Delayed Rectifier Conductance Shapes the Voltage Response of Type I Hair Cellsa A. J. RICCI, A. J. RICCI Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063 This work was supported by National Institutes of Health grant DC01273 (to M.J.C.). A.J.R. is a NASA Research Associate, K.J.R. is an NIH NRSA recipient, and M.J.C. is an NIH Clause Pepper investigator.Search for more papers by this authorK. J. RENNIE, K. J. RENNIE Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063Search for more papers by this authorM. J. CORREIA, Corresponding Author M. J. CORREIA Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063 Department of Physiology and Biophysics University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063e Corresponding author.Search for more papers by this author A. J. RICCI, A. J. RICCI Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063 This work was supported by National Institutes of Health grant DC01273 (to M.J.C.). A.J.R. is a NASA Research Associate, K.J.R. is an NIH NRSA recipient, and M.J.C. is an NIH Clause Pepper investigator.Search for more papers by this authorK. J. RENNIE, K. J. RENNIE Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063Search for more papers by this authorM. J. CORREIA, Corresponding Author M. J. CORREIA Department of Otolaryngology, University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063 Department of Physiology and Biophysics University of Texas Medical Branch at Galveston Galveston, Texas 77555–1063e Corresponding author.Search for more papers by this author First published: June 1996 https://doi.org/10.1111/j.1749-6632.1996.tb15761.xCitations: 3 c Current address: Department of Neurophysiology, University of Wisconsin, 1300 University Avenue, Madison, WI 53706. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume781, Issue1New Directions in Vestibular ResearchJune 1996Pages 690-692 RelatedInformation

Voltage-sensitive potassium channels in Drosophila photoreceptors

A preparation of dissociated Drosophila ommatidia is described that allows single-channel and whole-cell patch-clamp analysis of currents in identified sensory neurons. Three distinct classes of voltage-sensitive potassium conductances are characterized; all were detected in distal parts of ommatidia from sevenless mutants and hence in one cell class (R1-6 photoreceptors). Rapidly inactivating A-channels (IA), coded by the Shaker gene, were isolated in multichannel patches from adult flies. While showing similar kinetics to muscle A-channels, they differ from previously characterized wild-type Shaker channels in having a much more negative voltage operating range, being half-inactivated at approximately -70 mV. Two delayed rectifier conductances were characterized in whole-cell recordings from pupal photoreceptors. The most commonly encountered class (IKs) is similar to previously reported delayed rectifier conductances in Drosophila. It inactivates slowly (time constant, approximately 500 msec) and is half-inactivated at approximately -40 mV. A more rapidly inactivating delayed rectifier (IKf) was detected in approximately 30% of cells; it is half-inactivated at approximately -80 mV. Both IKs and IKf are blocked by 100 microM quinidine. Neither are greatly affected by 4-aminopyridine, which blocks IA at 1-5 mM. None of the three conductances was calcium dependent, nor were they obviously affected by the eag mutation, which affects K channels in muscle. The developmental profile of the channels is the inverse of that described in muscle. Both IKs and IKf are present at the earliest pupal stages examined (approximately 60 hr), but IA was only first detected at approximately 76 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Potassium conductance of the squid giant axon. Single-channel studies.

The patch-clamp technique was implemented in the cut-open squid giant axon and used to record single K channels. We present evidence for the existence of three distinct types of channel activities. In patches that contained three to eight channels, ensemble fluctuation analysis was performed to obtain an estimate of 17.4 pS for the single-channel conductance. Averaged currents obtained from these multichannel patches had a time course of activation similar to that of macroscopic K currents recorded from perfused squid giant axons. In patches where single events could be recorded, it was possible to find channels with conductances of 10, 20, and 40 pS. The channel most frequently encountered was the 20-pS channel; for a pulse to 50 mV, this channel had a probability of being open of 0.9. In other single-channel patches, a channel with a conductance of 40 pS was present. The activity of this channel varied from patch to patch. In some patches, it showed a very low probability of being open (0.16 for a pulse to 50 mV) and had a pronounced lag in its activation time course. In other patches, the 40-pS channel had a much higher probability of being open (0.75 at a holding potential of 50 mV). The 40-pS channel was found to be quite selective for K over Na. In some experiments, the cut-open axon was exposed to a solution containing no K for several minutes. A channel with a conductance of 10 pS was more frequently observed after this treatment. Our study shows that the macroscopic K conductance is a composite of several K channel types, but the relative contribution of each type is not yet clear. The time course of activation of the 20-pS channel and the ability to render it refractory to activation only by holding the membrane potential at a positive potential for several seconds makes it likely that it is the predominant channel contributing to the delayed rectifier conductance.