scholarly journals Whole-cell and single-channel currents activated by GABA and glycine in granule cells of the rat cerebellum.

1995 ◽  
Vol 485 (2) ◽  
pp. 419-435 ◽  
Author(s):  
M Kaneda ◽  
M Farrant ◽  
S G Cull-Candy
Keyword(s):  
Granule Cells ◽  
Single Channel ◽  
Whole Cell ◽  
Rat Cerebellum ◽  
Single Channel Currents ◽  
Channel Currents

scholarly journals Stretch-activated whole cell currents in adult rat cardiac myocytes

2000 ◽  
Vol 278 (2) ◽  
pp. H548-H557 ◽  
Author(s):  
Tao Zeng ◽  
Glenna C. L. Bett ◽  
Frederick Sachs
Keyword(s):  
Single Channel ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Cell Voltage ◽  
Cellular Level ◽  
Whole Cell ◽  
Adult Rat ◽  
Longitudinal Stretch ◽  
Single Channel Currents ◽  
Channel Currents

Mechanoelectric transduction can initiate cardiac arrhythmias. To examine the origins of this effect at the cellular level, we made whole cell voltage-clamp recordings from acutely isolated rat ventricular myocytes under controlled strain. Longitudinal stretch elicited noninactivating inward cationic currents that increased the action potential duration. These stretch-activated currents could be blocked by 100 μM Gd3+ but not by octanol. The current-voltage relationship was nearly linear, with a reversal potential of approximately −6 mV in normal Tyrode solution. Current density varied with sarcomere length (SL) according to I (pA/pF) = 8.3 − 5.0SL (μm). Repeated attempts to record single channel currents from stretch-activated ion channels failed, in accord with the absence of such data from the literature. The inability to record single channel currents may be a result of channels being located on internal membranes such as the T tubules or, possibly, inactivation of the channels by the mechanics of patch formation.

A microscope stage temperature controller for the study of whole-cell or single-channel currents

1985 ◽  
Vol 404 (4) ◽  
pp. 374-377 ◽  
Author(s):  
Lee D. Chabala ◽  
Robert E. Sheridan ◽  
David C. Hodge ◽  
John N. Power ◽  
Michael P. Walsh
Keyword(s):  
Single Channel ◽  
Whole Cell ◽  
Temperature Controller ◽  
Single Channel Currents ◽  
Channel Currents ◽  
Microscope Stage

Single-channel and whole-cell currents evoked by acetylcholine in dissociated sympathetic neurons of the rat

1987 ◽  
Vol 232 (1267) ◽  
pp. 239-248 ◽  
Keyword(s):  
Single Channel ◽  
Divalent Cations ◽  
Sympathetic Neurons ◽  
Outward Current ◽  
Inward Rectification ◽  
Normal Medium ◽  
Whole Cell ◽  
Old Rats ◽  
Single Channel Currents ◽  
Channel Currents

Single acetylcholine-activated channels have been recorded from neurons dissociated from the sympathetic chain of 17–21 day old rats. The mean single channel conductance is 35 pS in normal medium containing 1 mM calcium, and 51 pS in the absence of calcium. The measured current amplitudes are about five times more variable than at the frog endplate, at least in part because the current, while the channel is open, is much noisier than when it is shut. Single activations of the receptor by acetylcholine (ACh) produce a burst of openings; the distribution of the burst length has two components, the longer of which is of primary importance in synaptic transmission. Whole-cell currents, in response to ACh (up to 30 μM), show strong inward rectification with no outward current being detectable. This phenomenon is similar whether the intracellular ion is sodium or cesium, whether or not divalent cations are present, and whether or not atropine is present. Nevertheless, outward single-channel currents (of normal conductance) are detectable in isolated outside-out patches.

PKC activity modulates availability and long openings of L-type Ca2+ channels in A7r5 cells

1998 ◽  
Vol 275 (2) ◽  
pp. C535-C543 ◽  
Author(s):  
C. A. Obejero-Paz ◽  
M. Auslender ◽  
A. Scarpa
Keyword(s):  
Okadaic Acid ◽  
Single Channel ◽  
Inhibitory Effect ◽  
Patch Clamp Technique ◽  
Open Probability ◽  
Whole Cell ◽  
A7r5 Cells ◽  
High Level ◽  
Single Channel Currents ◽  
Channel Currents

The possibility that protein kinase C (PKC) could control the activity of L-type Ca2+ channels in A7r5 vascular smooth muscle-derived cells in the absence of agonist stimulation was investigated using the patch-clamp technique. Consistent with the possibility that L-type Ca2+ channels are maximally phosphorylated by PKC under these conditions, we show that 1) activation of PKC with the phorbol ester phorbol 12,13-dibutyrate was ineffective in modulating whole cell and single-channel currents, 2) inhibition of PKC activity with staurosporine or chelerythrine inhibited channel activity, 3) inhibition of protein phosphatases by intracellular dialysis of okadaic acid did not affect whole cell currents, and 4) the inhibitory effect of staurosporine was absent in the presence of okadaic acid. The inhibition of Ca2+ currents by PKC inhibitors was due to a decrease in channel availability and long open events, whereas the voltage dependence of the open probability and the single-channel conductance were not affected. The evidence suggests that in resting, nonstimulated A7r5 cells there is a high level of PKC activity that modulates the gating of L-type Ca2+ channels.

Sign in / Sign up

Export Citation Format

Share Document