%0 Journal Article %1 Jose_2002_2575 %A Josephson, Ira R %A Guia, Antonio %A Lakatta, Edward G %A Stern, Michael D %D 2002 %J Biophys J %K Animals; Barium, Calcium Calcium, Cells, Channels, Cultured; Electrophysiology; Factors Ions; Kinetics; L-Type, Male; Myocardium, Rats, Rats; Sprague-Dawley; Time chemistry/metabolism; chemistry; cytology; %N 5 %P 2575--2586 %T Modulation of the gating of unitary cardiac L-type Ca(2+) channels by conditioning voltage and divalent ions. %U http://www.biophysj.org/cgi/content/full/83/5/2575 %V 83 %X Although a considerable number of studies have characterized inactivation and facilitation of macroscopic L-type Ca(2+) channel currents, the single channel properties underlying these important regulatory processes have only rarely been examined using Ca(2+) ions. We have compared unitary L-type Ca(2+) channel currents recorded with a low concentration of Ca(2+) ions with those recorded with Ba(2+) ions to elucidate the ionic dependence of the mechanisms responsible for the prepulse-dependent modulation of Ca(2+) channel gating kinetics. Conditioning prepulses were applied across a wide range of voltages to examine their effects on the subsequent Ca(2+) channel activity, recorded at a constant test potential. All recordings were made in the absence of any Ca(2+) channel agonists. Moderate-depolarizing prepulses resulted in a decrease in the probability of opening of the Ca(2+) channels during subsequent test voltage steps (inactivation), the extent of which was more dramatic with Ca(2+) ions than Ba(2+) ions. Facilitation, or increase of the average probability of opening with strong predepolarization, was due to long-duration mode 2 openings with Ca(2+) ions and Ba(2+) ions, despite a decrease in Ca(2+) channel availability (inactivation) under these conditions. The degree of both prepulse-induced inactivation and facilitation decreased with increasing Ba(2+) ion concentration. The time constants (and their proportions) describing the distributions of Ca(2+) channel open times (which reflect mode switching) were also prepulse-, and ion-dependent. These results support the hypothesis that both prior depolarization and the nature and concentration of permeant ions modulate the gating properties of cardiac L-type Ca(2+) channels.

@article{Jose_2002_2575, abstract = {Although a considerable number of studies have characterized inactivation and facilitation of macroscopic L-type Ca(2+) channel currents, the single channel properties underlying these important regulatory processes have only rarely been examined using Ca(2+) ions. We have compared unitary L-type Ca(2+) channel currents recorded with a low concentration of Ca(2+) ions with those recorded with Ba(2+) ions to elucidate the ionic dependence of the mechanisms responsible for the prepulse-dependent modulation of Ca(2+) channel gating kinetics. Conditioning prepulses were applied across a wide range of voltages to examine their effects on the subsequent Ca(2+) channel activity, recorded at a constant test potential. All recordings were made in the absence of any Ca(2+) channel agonists. Moderate-depolarizing prepulses resulted in a decrease in the probability of opening of the Ca(2+) channels during subsequent test voltage steps (inactivation), the extent of which was more dramatic with Ca(2+) ions than Ba(2+) ions. Facilitation, or increase of the average probability of opening with strong predepolarization, was due to long-duration mode 2 openings with Ca(2+) ions and Ba(2+) ions, despite a decrease in Ca(2+) channel availability (inactivation) under these conditions. The degree of both prepulse-induced inactivation and facilitation decreased with increasing Ba(2+) ion concentration. The time constants (and their proportions) describing the distributions of Ca(2+) channel open times (which reflect mode switching) were also prepulse-, and ion-dependent. These results support the hypothesis that both prior depolarization and the nature and concentration of permeant ions modulate the gating properties of cardiac L-type Ca(2+) channels.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Josephson, Ira R and Guia, Antonio and Lakatta, Edward G and Stern, Michael D}, biburl = {https://www.bibsonomy.org/bibtex/22b916ea49785f9eb43c2a6b258666e0a/hake}, description = {The whole bibliography file I use.}, file = {Jose_2002_2575.pdf:Jose_2002_2575.pdf:PDF}, institution = {Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA. josephsoni@grc.nia.nih.gov}, interhash = {62706b5b5e818d5f750bb4605097edac}, intrahash = {2b916ea49785f9eb43c2a6b258666e0a}, journal = {Biophys J}, keywords = {Animals; Barium, Calcium Calcium, Cells, Channels, Cultured; Electrophysiology; Factors Ions; Kinetics; L-Type, Male; Myocardium, Rats, Rats; Sprague-Dawley; Time chemistry/metabolism; chemistry; cytology;}, month = Nov, number = 5, pages = {2575--2586}, pdf = {Jose_2002_2575.pdf}, pmid = {12414691}, timestamp = {2009-06-03T11:21:17.000+0200}, title = {Modulation of the gating of unitary cardiac L-type Ca(2+) channels by conditioning voltage and divalent ions.}, url = {http://www.biophysj.org/cgi/content/full/83/5/2575}, volume = 83, year = 2002 }