scholarly journals Blockage of the light-sensitive conductance in hyperpolarizing photoreceptors of the scallop. Effects of tetraethylammonium and 4-aminopyridine.

1994 ◽  
Vol 104 (3) ◽  
pp. 487-505 ◽  
Author(s):  
M D Gomez ◽  
E Nasi
Keyword(s):  
Potassium Channels ◽  
Light Sensitivity ◽  
Rapid Onset ◽  
Potassium Ions ◽  
The Family ◽  
Cell Recording ◽  
Voltage Dependent ◽  
A Site ◽  
Membrane Treatment ◽  
Phototransduction Cascade

The tight-seal whole-cell recording technique was used to examine the effect of tetraethylammonium (TEA) and 4-aminopyridine (4-AP) on the photocurrent of hyperpolarizing ciliary photoreceptors isolated from the distal retina of the bay scallop (Pecten irradians). In these cells, light causes an increase in a conductance that is highly selective to potassium ions. Extracellular application of TEA at a concentration of 50 mM produced a modest, reversible block (approximately 35% at -20 mV holding potential). The blockage was weakly voltage dependent, increasing by approximately 20% for a 20-mV hyperpolarization, suggestive of a site of interaction superficially located within the electric field of the membrane. Treatment with TEA produced no significant changes either in the light sensitivity of the photocurrent or in its kinetics. The effects of superfusion with 4-AP were more dramatic: the light-evoked current was nearly abolished (> 95%) at submillimolar concentrations, with a half-maximal dose of approximately 0.6 microns. The blockage had a rapid onset and was slowly reversible. No significant use or voltage dependency were observed. A number of control experiments indicated that the phototransduction cascade remained functional during treatment with 4-AP: the early receptor current, the prolonged after current and its suppression, the photoresponse kinetics and the light sensitivity of the cell were little affected by 4-AP, suggesting that the suppression of the photocurrent is due to blockage of the light-sensitive channels, rather than impairment of some of the activation steps. The results are discussed in the light of a possible kinship between the light-activated potassium channels of invertebrate hyperpolarizing photoreceptors and the family of rapidly-inactivating voltage-dependent potassium channels, which typically exhibit high susceptibility to blockage by this drug.

Influence of the external concentration of potassium ions on functioning of voltage-dependent potassium channels in GH3 cells

1995 ◽  
Vol 27 (2) ◽  
pp. 85-89 ◽  
Author(s):  
A. V. Grishchenko ◽  
N. M. Berezetskaya ◽  
G. E. Weinreb ◽  
N. I. Kononenko ◽  
M. B. Sedova
Keyword(s):  
Potassium Channels ◽  
Gh3 Cells ◽  
Potassium Ions ◽  
External Concentration ◽  
Voltage Dependent

scholarly journals Interaction between tetraethylammonium and amino acid residues in the pore of cloned voltage-dependent potassium channels.

1991 ◽  
Vol 266 (12) ◽  
pp. 7583-7587
Author(s):  
M P Kavanaugh ◽  
M D Varnum ◽  
P B Osborne ◽  
M J Christie ◽  
A E Busch ◽  
...  
Keyword(s):  
Amino Acid ◽  
Potassium Channels ◽  
Amino Acid Residues ◽  
Voltage Dependent

scholarly journals Activation-inactivation of potassium channels and development of the potassium-channel spike in internally perfused squid giant axons.

1981 ◽  
Vol 78 (1) ◽  
pp. 43-61 ◽  
Author(s):  
I Inoue
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Voltage Clamp ◽  
Time Constant ◽  
Equilibrium Potential ◽  
Giant Axons ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Time Courses ◽  
Calcium Permeability

A spike that is the result of calcium permeability through potassium channels was separated from the action potential is squid giant axons internally perfused with a 30 mM NaF solution and bathed in a 100 mM CaCl2 solution by blocking sodium channels with tetrodotoxin. Currents through potassium channels were studied under voltage clamp. The records showed a clear voltage-dependent inactivation of the currents. The inactivation was composed of at least two components; one relatively fast, having a time constant of 20--30 ms, and the other very slow, having a time constant of 5--10 s. Voltage clamp was carried out with a variety of salt compositions in both the internal and external solutions. A similar voltage-dependent inactivation, also composed of the two components, was recognized in all the current through potassium channels. Although the direction and intensity of current strongly depended on the salt composition of the solutions, the time-courses of these currents at corresponding voltages were very similar. These results strongly suggest that the inactivation of the currents in attributable to an essential, dynamic property of potassium channels themselves. Thus, the generation of a potassium-channel spike can be understood as an event that occurs when the equilibrium potential across the potassium channel becomes positive.

scholarly journals Voltage-dependent block of endothelial volume-regulated anion channels by calix[4]arenes

1998 ◽  
Vol 275 (3) ◽  
pp. C646-C652 ◽  
Author(s):  
Guy Droogmans ◽  
Jean Prenen ◽  
Jan Eggermont ◽  
Thomas Voets ◽  
Bernd Nilius
Keyword(s):  
Open Channel ◽  
Single Channel ◽  
Anion Channel ◽  
Anion Channels ◽  
Channel Conductance ◽  
Open Channel Block ◽  
Maximum Inhibition ◽  
Voltage Dependent ◽  
A Site ◽  
Maximal Block

We have studied the effects of calix[4]arenes on the volume-regulated anion channel (VRAC) currents in cultured calf pulmonary artery endothelial cells. TS- and TS-TM-calix[4]arenes induced a fast inhibition at positive potentials but were ineffective at negative potentials. Maximal block occurred at potentials between 30 and 50 mV. Lowering extracellular pH enhanced the block and shifted the maximum inhibition to more negative potentials. Current inhibition was also accompanied by an increased current noise. From the analysis of the calix[4]arene-induced noise, we obtained a single-channel conductance of 9.3 ± 2.1 pS ( n = 9) at +30 mV. The voltage- and time-dependent block were described using a model in which calix[4]arenes bind to a site at an electrical distance of 0.25 inside the channel with an affinity of 220 μM at 0 mV. Binding occludes VRAC at moderately positive potentials, but calix[4]arenes permeate the channel at more positive potentials. In conclusion, our data suggest an open-channel block of VRAC by calix[4]arenes that also depends on the protonation of the binding site within the pore.

Voltage dependence of conductance changes evoked by glycine release in the zebrafish brain

1995 ◽  
Vol 73 (6) ◽  
pp. 2404-2412 ◽  
Author(s):  
P. Legendre ◽  
H. Korn
Keyword(s):  
Voltage Dependence ◽  
Reversal Potential ◽  
Voltage Sensitivity ◽  
M Cell ◽  
Open Probability ◽  
Similar Time ◽  
Whole Cell ◽  
Glycine Release ◽  
Cell Recording ◽  
Voltage Dependent

1. The kinetics and mechanisms underlying the voltage dependence of inhibitory postsynaptic currents (IPSCs) recorded in the Mauthner cell (M cell) were investigated in the isolated medulla of 52-h-old zebrafish larvae, with the use of whole cell and outside-out patch-clamp recordings. 2. Spontaneous miniature IPSCs (mIPSCs) were recorded in the presence of 10(-6) M tetrodotoxin (TTX), 10 mM MgCl2, and 0.1 mM [CaCl2]o. Depolarizing the cell from -50 to +50 mV did not evoke any significant change in the distribution of mIPSC amplitudes, whereas synaptic currents were prolonged at positive voltages. The average decay time constant was increased twofold at +50 mV. 3. The voltage dependence of the kinetics of glycine-activated channels was first investigated during whole cell recording experiments. Currents evoked by voltage steps in the presence of glycine (50 microM) were compared with those obtained without glycine. The increase in chloride conductance (gCl-) evoked by glycine was time and voltage dependent. Inactivation and reactivation of the chloride current were observed during voltage pulses from 0 to -50 mV and from -50 to 0 mV, respectively, and they occurred with similar time constants (2-3 s). During glycine application, voltage-ramp analysis revealed a shift in the reversal potential (ECl-) occurring at all [Cl-]i tested. 4. The basis of the voltage sensitivity of glycine-evoked gCl- was first analyzed by measuring the relative changes in the total open probability (NPo) of glycine-activated channels with voltage.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential Oxidative Modulation of Voltage-Dependent K+ Currents in Rat Hippocampal Neurons

2002 ◽  
Vol 87 (6) ◽  
pp. 2990-2995 ◽  
Author(s):  
Wolfgang Müller ◽  
Katrin Bittner
Keyword(s):  
Hydrogen Peroxide ◽  
Hippocampal Neurons ◽  
Immune Defense ◽  
Delayed Rectifier ◽  
Delayed Rectifier Current ◽  
Cell Recording ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
K Currents ◽  
Stimulation Of

Oxidative stress is enhanced by [Ca2+]i-dependent stimulation of phospholipases and mitochondria and has been implicated in immune defense, ischemia, and excitotoxicity. Using whole cell recording from hippocampal neurons, we show that arachidonic acid (AA) and hydrogen peroxide (H2O2) both reduce the transient K+ current I A by −54 and −68%, respectively, and shift steady-state inactivation by −10 and −15 mV, respectively. While AA was effective at an extracellular concentration of 1 μM and an intracellular concentration of 1 pM, extracellular H2O2 was equally effective only at a concentration >800 μM (0.0027%). In contrast to AA, H2O2 decreased the slope of activation and increased the slope of inactivation of I A and reduced the sustained delayed rectifier current I K(V) by 22% and shifted its activation by −9 mV. Intracellular application of the antioxidant glutathione (GSH, 2–5 mM) blocked all effects of AA and the reduction of I A by H2O2. In contrast, intracellular GSH enhanced reduction of I K(V) by H2O2. Decrease of the slope of activation and increase of the slope of inactivation of I A by hydrogen peroxide was blocked and reversed to a decrease, respectively, by intracellular application of GSH. Intracellular GSH did not prevent H2O2 to shift inactivation and activation of I A and activation of I K(V) to more negative potentials. We conclude, that AA and H2O2modulate voltage-activated K currents differentially by oxidation of GSH accessible intracellular and GSH inaccessible extracellular K+-channel domains, thereby presumably affecting neuronal information processing and oxidative damage.

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