scholarly journals The effect of some anesthetics and natural venoms on the LCС-channels functioning of the nuclear membrane of cardiomyocytes and cerebellum Purkinje neurons

2019 ◽  
Vol 79 (3) ◽  
Author(s):  
O. Kotyk ◽  
A. Kotliarova ◽  
O. Isaeva ◽  
S. Marchenko
Keyword(s):  
Nuclear Membrane ◽  
Purkinje Neurons ◽  
Average Amplitude ◽  
Biophysical Parameters ◽  
Patch Clamp Technique ◽  
Physiological Relevance ◽  
K Current ◽  
Patch Configuration ◽  
High Concentrations ◽  
Cerebellar Purkinje Neurons

The investigation of pharmacological sensitivity of the cationic channels in nuclear membrane to the influence of anesthetics and natural venoms is relevant since it was shown that some modulators of N-cholinoreceptors (dithylinum, atracurium) affecting the large conductance cation channels (LCC-channels) functional activity are used in medicine during surgery. In addition, some injectable forms of toxins from the snake venom are used as drugs with an analgesic effect. Therefore, the aim of the study was to investigate the pharmacological sensitivity of the LCC-channels to the muscle relaxants, anaesthetics (mydocalm, diprofol) and natural venoms (neurotoxin II, α-Cobratoxin). The influence of these substances was evaluated based on changes in biophysical parameters of functioning of the LCC-channels of nuclear membrane of the cardiomyocytes and cerebellar Purkinje neurons. Ion currents through these channels were registered in the nucleus-attached or excised patch configuration and the voltage-clamp mode of the patch-clamp technique. We found that mydocalm (2 mM), diprofol (2 mM) and α-Cobratoxin (1 mM) reduced several times the probability of the channels being in the open state. Under the influence of mydocalm and α-Kobratoxin in high concentrations (1-2 mM) the effect of channels flickering was observed which indicates the channel pore blocking in its open state. At the same time, the average amplitude of the K+ current through the LCC-channels decreased by 13 % under the influence of NT II (25 μM). The results will be the basis for identification of new, more effective inhibitors of the LCC-channels that will be promising for the physiological relevance and structure of the channels investigation.

Spontaneous transient outward currents and delayed rectifier K+ current: effects of hypoxia

1998 ◽  
Vol 275 (1) ◽  
pp. L145-L154 ◽  
Author(s):  
C. Vandier ◽  
M. Delpech ◽  
P. Bonnet
Keyword(s):  
Steady State ◽  
Outward Current ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Outward Currents ◽  
K Current ◽  
The Mean ◽  
Patch Configuration ◽  
Spontaneous Transient Outward Currents ◽  
Dependent Mechanism

Single smooth muscle cells of rabbit intrapulmonary artery were voltage clamped using the perforated-patch configuration of the patch-clamp technique. We observed spontaneous transient outward currents (STOCs) and a steady-state outward current. Because STOCs were tetraethylammonium sensitive and activated by Ca2+ influx, they were believed to represent activation of Ca2+-activated K+ channels. The steady-state outward current, which was sensitive to 4-aminopyridine, was the delayed rectifier K+ current. In cells voltage clamped at 0 mV, we found that STOCs were not randomly distributed in amplitude but were composed of multiples of 1.57 ± 0.56 pA/pF. The mean frequency of STOCs was 5.51 ± 3.49 Hz. Ryanodine (10 μM), caffeine (5 mM), thapsigargin (200 nM), and hypoxia [Formula: see text] = 10 mmHg) decreased STOCs. The effect of hypoxia on STOCs was partially reversible only if the experiment was conducted in the presence of thapsigargin. Hypoxia and thapsigargin decrease steady-state outward current. Thapsigargin and removal of external Ca2+abolished the effect of hypoxia, suggesting that hypoxia decreases steady-state outward current by a Ca2+-dependent mechanism.

Expression of CFTR controls cAMP-dependent activation of epithelial K+ currents

1996 ◽  
Vol 271 (5) ◽  
pp. C1565-C1573 ◽  
Author(s):  
G. Loussouarn ◽  
S. Demolombe ◽  
R. Mohammad-Panah ◽  
D. Escande ◽  
I. Baro
Keyword(s):  
Cftr Gene ◽  
High Concentration ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Transfected Cells ◽  
Cyclic Monophosphate ◽  
K Current ◽  
Patch Configuration ◽  
Camp Stimulation ◽  
K Currents

The perforated-patch configuration of the patch-clamp technique was used to record whole cell currents from human epithelial CFPAC-1 cells defective for functional cystic fibrosis transmembrane conductance regulator (CFTR). In CFPAC-1 cells, adenosine 3',5'-cyclic monophosphate (cAMP) stimulation with forskolin (10 microM) plus 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate (400 microM) activated neither Cl- nor K+ currents. In the same cells transfected with wild-type CFTR gene, cAMP stimulation produced activation of both Cl- and K+ currents. In Cl(-)-depleted medium (gluconate as a substitute), cAMP stimulation evoked a K+ current in CFTR-transfected but not in untransfected CFPAC-1 cells. This cAMP-evoked K+ current was the sum of two components: 1) a time-independent inwardly rectifying component, and 2) a slowly relaxing component activated at positive voltages. Increasing intracellular Ca2+ with ionomycin (1 microM) activated K+ currents in either transfected or untransfected cells. In transfected cells, blocking the CFTR conductance with high-concentration glibenclamide (100 microM) reduced the K+ current when activated by cAMP but not when activated by Ca2+. Pretreating CFTR-transfected cells for 48 h with interferon-gamma downregulated CFTR gene expression and reduced cAMP but not Ca2+ activation of the whole cell K+ current. From these results, we conclude that functional membrane CFTR protein influences activation by cAMP of epithelial K+ currents.

scholarly journals Continuous network of endoplasmic reticulum in cerebellar Purkinje neurons.

1994 ◽  
Vol 91 (16) ◽  
pp. 7510-7514 ◽  
Author(s):  
M. Terasaki ◽  
N. T. Slater ◽  
A. Fein ◽  
A. Schmidek ◽  
T. S. Reese
Keyword(s):  
Endoplasmic Reticulum ◽  
Purkinje Neurons ◽  
Cerebellar Purkinje Neurons

L‐type Ca 2+ channels contribute to current‐evoked spike firing and associated Ca 2+ signals in cerebellar Purkinje neurons

2006 ◽  
Vol 5 (2) ◽  
pp. 146-154 ◽  
Author(s):  
D. L. Gruol ◽  
J. G. Netzeband ◽  
J. Schneeloch ◽  
C. E. Gullette
Keyword(s):  
Purkinje Neurons ◽  
Cerebellar Purkinje Neurons ◽  
Spike Firing

scholarly journals Modulation of membrane currents by cyclic AMP in cleavage-arrested Drosophila neurons.

1996 ◽  
Vol 199 (3) ◽  
pp. 537-548
Author(s):  
W B Alshuaib ◽  
L Byerly
Keyword(s):  
Cyclic Amp ◽  
Membrane Currents ◽  
K Channel ◽  
Neuronal Membrane ◽  
Patch Clamp Technique ◽  
Large Variability ◽  
Whole Cell ◽  
Intracellular Environment ◽  
K Current ◽  
Channel Currents

A number of Drosophila learning mutants have defective intracellular second-messenger systems. In an effort to develop techniques that will allow direct measurement of the effects of these mutations on whole-cell neuronal membrane currents, the perforated-patch whole-cell (PPWC) technique has been applied to cleavage-arrested cultured embryonic Drosophila neurons. This technique permits the measurement of membrane currents without disturbing the intracellular environment. As a result of the maintenance of the intracellular environment, Drosophila neuron currents are found to be much more stable than when measured using the conventional whole-cell (CWC) patch-clamp technique. Ca2+ channel currents, which typically 'wash out' within a few minutes of the beginning of CWC recording, are stable for the duration of the seal (tens of minutes) when measured using the PPWC technique. Since the learning mutations dunce and rutabaga disrupt cyclic AMP signalling, the action of externally applied dibutyryl cyclic AMP (db-cAMP) and theophylline on Ca2+ and K+ channel currents were studied. db-cAMP and theophylline enhanced the Ba2+ current, carried by Ca2+ channels, but had no effect on the K+ current in the cleavage-arrested neurons. However, the large variability and reduction in density of Ba2+ and K+ currents raise questions about the suitability of using these cleavage-arrested cells as models for Drosophila neurons.

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