Reply: Possible effects of reduced conductance in delayed-rectifier K+ current on neuronal activity

2012 ◽  
Vol 27 (12) ◽  
pp. 1583-1583
Author(s):  
Erwin B. Montgomery
Keyword(s):  
Neuronal Activity ◽  
Delayed Rectifier ◽  
K Current

scholarly journals Basal and angiotensin II-inhibited neuronal delayed-rectifier K+ current are regulated by thioredoxin

2007 ◽  
Vol 293 (1) ◽  
pp. C211-C217 ◽  
Author(s):  
Tomokazu Matsuura ◽  
Rachael A. Harrison ◽  
Andrew D. Westwell ◽  
Hajime Nakamura ◽  
Anatoly E. Martynyuk ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Negative Regulator ◽  
General Mechanism ◽  
Delayed Rectifier ◽  
Neuronal Cultures ◽  
Ang Ii ◽  
Small Proteins ◽  
K Current ◽  
Thiol Protein ◽  
Negative Regulatory Role

In previous studies, we determined that macrophage migration inhibitory factor (MIF), acting intracellularly via its intrinsic thiol-protein oxidoreductase (TPOR) activity, stimulates basal neuronal delayed-rectifier K+ current ( IKv) and inhibits basal and angiotensin (ANG) II-induced increases in neuronal activity. These findings are the basis for our hypothesis that MIF is a negative regulator of ANG II actions in neurons. MIF has recently been recategorized as a member of the thioredoxin (Trx) superfamily of small proteins. In the present study we have examined whether Trx influences basal and ANG II-modulated IKv in an effort to determine whether the Trx superfamily can exert a general regulatory influence over neuronal activity and the actions of ANG II. Intracellular application of Trx (0.8–80 nM) into rat hypothalamic/brain stem neurons in culture increased neuronal IKv, as measured by voltage-clamp recordings. This effect of Trx was abolished in the presence of the TPOR inhibitor PMX 464 (800 nM). Furthermore, the mutant protein recombinant human C32S/C35S-Trx, which lacks TPOR activity, failed to alter neuronal IKv. Trx applied at a concentration (0.08 nM) that does not alter basal IKv abolished the inhibition of neuronal IKv produced by ANG II (100 nM). Given our observation that ANG II increases Trx levels in neuronal cultures, it is possible that Trx (like MIF) has a negative regulatory role over basal and ANG II-stimulated neuronal activity via modulation of IKv. Moreover, these data suggest that TPOR may be a general mechanism for negatively regulating neuronal activity.

scholarly journals Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties

2021 ◽  
Vol 14 (8) ◽  
pp. 748
Author(s):  
Péter P. Nánási ◽  
Balázs Horváth ◽  
Fábián Tar ◽  
János Almássy ◽  
Norbert Szentandrássy ◽  
...  
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Laboratory Animals ◽  
Delayed Rectifier ◽  
Ion Currents ◽  
Human Cardiomyocytes ◽  
Ventricular Cells ◽  
Repolarization Reserve ◽  
Electrophysiological Studies ◽  
K Current

Due to the limited availability of healthy human ventricular tissues, the most suitable animal model has to be applied for electrophysiological and pharmacological studies. This can be best identified by studying the properties of ion currents shaping the action potential in the frequently used laboratory animals, such as dogs, rabbits, guinea pigs, or rats, and comparing them to those of human cardiomyocytes. The authors of this article with the experience of three decades of electrophysiological studies, performed in mammalian and human ventricular tissues and isolated cardiomyocytes, summarize their results obtained regarding the major canine and human cardiac ion currents. Accordingly, L-type Ca2+ current (ICa), late Na+ current (INa-late), rapid and slow components of the delayed rectifier K+ current (IKr and IKs, respectively), inward rectifier K+ current (IK1), transient outward K+ current (Ito1), and Na+/Ca2+ exchange current (INCX) were characterized and compared. Importantly, many of these measurements were performed using the action potential voltage clamp technique allowing for visualization of the actual current profiles flowing during the ventricular action potential. Densities and shapes of these ion currents, as well as the action potential configuration, were similar in human and canine ventricular cells, except for the density of IK1 and the recovery kinetics of Ito. IK1 displayed a largely four-fold larger density in canine than human myocytes, and Ito recovery from inactivation displayed a somewhat different time course in the two species. On the basis of these results, it is concluded that canine ventricular cells represent a reasonably good model for human myocytes for electrophysiological studies, however, it must be borne in mind that due to their stronger IK1, the repolarization reserve is more pronounced in canine cells, and moderate differences in the frequency-dependent repolarization patterns can also be anticipated.

Clofilium-induced Block of Delayed Rectifier Type K+Current in Atrial Tumor Cells (AT-1 Cells)

1997 ◽  
Vol 29 (1) ◽  
pp. 301-307 ◽  
Author(s):  
Mohit Lal Bhattacharyya ◽  
Shukla Sarker ◽  
Kawonia P Mull ◽  
Qadriyyah Debnam
Keyword(s):  
Tumor Cells ◽  
Delayed Rectifier ◽  
Type K ◽  
K Current ◽  
Atrial Tumor

scholarly journals Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents.

1990 ◽  
Vol 96 (1) ◽  
pp. 195-215 ◽  
Author(s):  
M C Sanguinetti ◽  
N K Jurkiewicz
Keyword(s):  
Antiarrhythmic Agent ◽  
Reversal Potential ◽  
Differential Sensitivity ◽  
Inward Rectification ◽  
Delayed Rectifier ◽  
Antiarrhythmic Agents ◽  
Class Iii ◽  
Activation Curve ◽  
Voltage Range ◽  
K Current

An envelope of tails test was used to show that the delayed rectifier K+ current (IK) of guinea pig ventricular myocytes results from the activation of two outward K+ currents. One current was specifically blocked by the benzenesulfonamide antiarrhythmic agent, E-4031 (IC50 = 397 nM). The drug-sensitive current, "IKr" exhibits prominent rectification and activates very rapidly relative to the slowly activating drug-insensitive current, "IKs." IKs was characterized by a delayed onset of activation that occurs over a voltage range typical of the classically described cardiac IK. Fully activated IKs, measured as tail current after 7.5-s test pulses, was 11.4 times larger than the fully activated IKr. IKr was also blocked by d-sotalol (100 microM), a less potent benzenesulfonamide Class III antiarrhythmic agent. The activation curve of IKr had a steep slope (+7.5 mV) and a negative half-point (-21.5 mV) relative to the activation curve of IKs (slope = +12.7 mV, half-point = +15.7 mV). The reversal potential (Erev) of IKr (-93 mV) was similar to EK (-94 mV for [K+]o = 4 mM), whereas Erev of IKs was -77 mV. The time constants for activation and deactivation of IKr made up a bell-shaped function of membrane potential, peaking between -30 and -40 mV (170 ms). The slope conductance of the linear portion of the fully activated IKr-V relation was 22.5 S/F. Inward rectification of this relation occurred at potentials greater than -50 mV, resulting in a voltage-dependent decrease in peak IKr at test potentials greater than 0 mV. Peak IKr at 0 mV averaged 0.8 pA/pF (n = 21). Although the magnitude of IKr was small relative to fully activated IKs, the two currents were of similar magnitude when measured during a relatively short pulse protocol (225 ms) at membrane potentials (-20 to +20 mV) typical of the plateau phase of cardiac action potentials.

Brain natriuretic peptide modulates the delayed rectifier outward K+ current and promotes the proliferation of mouse schwann cells

2010 ◽  
Vol 226 (2) ◽  
pp. 440-449 ◽  
Author(s):  
Xiao-Wei Fei ◽  
Chen-Jie Pan ◽  
Yan-Lin He ◽  
Yan-Jia Fang ◽  
Jia-Li Zhuang ◽  
...  
Keyword(s):  
Brain Natriuretic Peptide ◽  
Schwann Cells ◽  
Natriuretic Peptide ◽  
Delayed Rectifier ◽  
K Current

scholarly journals Histamine H1 -receptor-mediated modulation of the delayed rectifier K+ current in guinea-pig atrial cells: opposite effects on IKs and IKr

1999 ◽  
Vol 128 (7) ◽  
pp. 1545-1553 ◽  
Author(s):  
Yasunori Matsumoto ◽  
Takehiko Ogura ◽  
Hiroko Uemura ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Delayed Rectifier ◽  
H1 Receptor ◽  
Histamine H1 Receptor ◽  
Atrial Cells ◽  
K Current

Na+, K+ and Ca2+ currents in identified leech neurones in culture

1989 ◽  
Vol 141 (1) ◽  
pp. 1-20
Author(s):  
R. R. Stewart ◽  
J. G. Nicholls ◽  
W. B. Adams
Keyword(s):  
Minor Component ◽  
Outward Current ◽  
Membrane Properties ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Channel Blockers ◽  
Sensory Neurones ◽  
K Current ◽  
The Individual ◽  
K Currents

1. Na+, K+ and Ca2+ currents have been measured by voltage-clamp in Retzius (R), anterior pagoda (AP) and sensory (pressure, touch and nociceptive) cells dissected from the central nervous system (CNS) of the leech. These cells maintain their distinctive membrane properties and action potential configurations in culture. Currents carried by the individual ions were analysed by the use of channel blockers and by their kinetics. Since the cells are isopotential they can be voltage-clamped effectively. 2. Depolarization, as expected, gave rise to an early inward Na+ current followed by a delayed outward K+ current. In Na+-free medium containing tetraethylammonium (TEA+), and in the presence of 4-aminopyridine (4-AP), inward Ca2+ currents were revealed that inactivated slowly and were blocked by Cd2+ and Mn2+. 3. Na+ and Ca2+ currents were similar in their characteristics in R. AP and sensory neurones. In contrast, K+ currents showed marked differences. Three principal K+ currents were identified. These differed in their time courses of activation and inactivation and in their responses to Ca2+ channel blockers. 4. K+ currents of the A-type (IA) activated and inactivated rapidly, were not affected by Ca2+ channel blockers and were eliminated by steady-state inactivation at holding potentials of −30 mV. A-type K+ currents were found in AP cells and as a minor component of the outward current in R cells. A Ca2+-activated K+ current (IC), that inactivated more slowly and was reduced by Ca2+ channel blockers, constituted the major outward current in R cells. The third K+ current resembled the delayed rectifier currents (IK1 and IK2) of squid axons with slow activation and inactivation kinetics. Such currents were found in R cells and in the sensory neurones (T, P and N). 5. The principal differences in membrane properties of identified leech neurones can be explained in terms of the numbers of Na+ channels and the distinctive kinetics of K+ channels in each type of cell.

scholarly journals Sulfhydryl modification affects coronary artery tension by changing activity of delayed rectifier K+current

2000 ◽  
Vol 41 (3) ◽  
pp. 372 ◽  
Author(s):  
Miyong Ha ◽  
Sungchoon Kwon ◽  
Young Ho Lee ◽  
Dongsoo Yeon ◽  
Duck Sun Ahn
Keyword(s):  
Coronary Artery ◽  
Delayed Rectifier ◽  
Sulfhydryl Modification ◽  
K Current
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