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PubMed1995

Electrophysiological effects of Ro 22-9194, a new antiarrhythmic agent, on guinea-pig ventricular cells.

1. Cardiac effects of Ro 22-9194 were examined in papillary muscles and single ventricular myocytes isolated from guinea-pigs and compared with those of moricizine. 2. In papillary muscles, both Ro 22-9194 (> or = 10 microM) and moricizine (> or = 1 microM) caused a significant dose-dependent decrease in the maximum upstroke velocity (Vmax) and a shortening of the action potential duration. 3. In the presence of either drug, trains of stimuli at rates > or = 0.2 Hz led to an exponential decline in Vmax. This use-dependent block was enhanced at higher stimulation frequencies. A time constant (tau R) for Vmax recovery from the use-dependent block was 9.3 s for Ro 22-9194 and 26.4 s for moricizine. 4. The curves relating membrane potential and Vmax in single myocytes were shifted by Ro 22-9194 (30 microM) or by moricizine (3 microM) in a hyperpolarizing direction by 8.4 mV and 8.0 mV respectively. 5. In myocytes treated with Ro 22-9194 (30 microM), a 10 ms conditioning clamp to 0 mV caused a significant decrease in Vmax of the subsequent test action potential; further prolongation of the clamp pulse duration resulted in a modest enhancement of the Vmax inhibition. In the presence of moricizine (3 microM), a similar conditioning clamp > 200 ms caused a significant Vmax reduction; the longer the clamp pulse duration, the greater the Vmax reduction. 6. Ro 22-9194 > or = 30 microM caused a slight decrease of calcium inward current (ICa) of myocytes without affecting the delayed rectifier potassium current (IK). 7. These findings suggest that the primary electrophysiological effect of Ro 22-9194 as an antiarrhythmicagent is, like moricizine, a use- and voltage-dependent inhibition of sodium channels. From the onset and offset kinetics of the use-dependent block, Ro 22-9194 belongs to the intermediate kinetic Class I drugs, while moricizine is a slow kinetic drug. From the state-dependence of sodium channel block, Ro 22-9194 may belong to activated channel blockers, while moricizine belongs to inactivated channel blockers.

Action Potentials↗
PubMed2004

The protein tyrosine kinase inhibitor, genistein, decreases excitability of nociceptive neurons.

One mechanism by which neurons regulate their excitability is through ion channel phosphorylation. Compounds that increase nociceptive neuron excitability can cause hyperalgesia or allodynia whereas compounds that decrease nociceptive neuron excitability can be used as analgesics to relieve pain arising from inflammation or trauma. To identify targets that may cause a decrease in nociceptive neuron excitability, we have investigated the effects of genistein, a specific inhibitor of protein tyrosine kinases (PTKs), on capsaicin-sensitive neurons from cultured rat trigeminal ganglion neurons. It was found that genistein decreased the number of evoked action potentials, and hence their excitability. To determine whether genistein's effects occur through the inhibition of PTKs, we also tested the effects of two of its inactive analogues, daidzein and genistin. Whereas daidzein decreased excitability, albeit to a lower extent than genistein, excitability was unaffected by genistin. To determine which currents are involved in genistein's reduction in nociceptive neuron excitability, whole-cell voltage-clamp measurements were performed on voltage-gated sodium and potassium currents. One hundred micromolar genistein, daidzein and genistin inhibited tetrodotoxin-resistant voltage-gated sodium currents 74, 42, and 3%, respectively. Genistein markedly inhibited delayed rectifier (IK) and IA potassium currents, whereas daidzein and genistin were comparatively ineffective. In summary, we found that genistein's ability to inhibit nociceptive neuron excitability arises primarily from its non-specific inhibition of voltage-dependent sodium channels.

Action Potentials↗
PubMed2003

What are the roles of the many different types of potassium channel expressed in cerebellar granule cells?

Potassium (K) channels have a key role in the regulation of neuronal excitability. Over a hundred different subunits encoding distinct K channel subtypes have been identified so far. A major challenge is to relate these many different channel subunits to the functional K currents observed in native neurons. In this review, we have concentrated on cerebellar granule neurons (CGNs). We have considered each of the three principal super families of K channels in turn, namely, the six transmembrane domain, voltage-gated super family, the two transmembrane domain, inward-rectifier super family and the four transmembrane domain, leak channel super family. For each super family, we have identified the subunits that are expressed in CGNs and related the properties of these expressed channel subunits to the functional currents seen in electrophysiological recordings from these neurons. In some cases, there are strong molecular candidates for proteins underlying observed currents. In other cases the correlation is less clear. We show that at least 26 potassium channel alpha subunits are moderately or strongly expressed in CGNs. Nevertheless, a good empirical model of CGN function has been obtained with just six distinct K conductances. The transient KA current in CGNs, seems due to expression of Kv4.2 channels or Kv4.2/4.3 heteromers, while the KCa current is due to expression of large-conductance slo channels. The G-protein activated KIR current is probably due to heteromeric expression of KIR3.1 and KIR3.2. Perhaps KIR2.2 subunits underlie the KIR current when it is constitutively active. The leak conductance can be attributed to TASK-1 and or TASK-3 channels. With less certainty, the IK-slow current may be due to expression of one or more members of the KCNQ or EAG family. Lastly, the delayed-rectifier Kv current has as many as six different potential contributors from the extensive Kv family of alpha subunits. Since many of these subunits are highly regulated by neurotransmitters, physiological regulators and, often, auxiliary subunits, the resulting electrical properties of CGNs may be highly dynamic and subject to constant fine-tuning.

Animals↗
PubMed2026

GIRK Channels Regulate Circadian Rhythms of Excitability in Prokineticin 2 Neurons of the Suprachiasmatic Nucleus and Modulate Behavioral Circadian Rhythms.

The suprachiasmatic nucleus (SCN), the central circadian clock in mammals, generates robust yet adaptable circadian rhythms through electrically mediated coordination among heterogeneous peptidergic neuronal populations with presumed cell type-specific roles. Previous studies have proposed that circadian changes in membrane excitability of individual SCN neurons arise from time-of-day-dependent shifts in the relative balance of subthreshold Na+ and K+ conductances. Although multiple channels have been implicated in these processes, how nocturnally dominant K+ conductances are implemented in a cell type-specific manner remains poorly understood. Prokineticin 2 (Prok2) has been identified as a SCN signaling peptide essential for behavioral circadian regulation; however, the electrophysiological properties of Prok2-expressing neurons and the mechanisms underlying their diurnal rhythmicity remain largely unexplored. Here, using electrophysiological approaches in mice of either sex, we show that Prok2 neurons exhibit diurnal variations in electrical properties, with higher excitability during the day and reduced excitability at night, and that G-protein-coupled inwardly rectifying potassium (GIRK) channel-mediated basal current contributes to nighttime hyperpolarization. Immunofluorescence and single-cell RT-PCR analyses revealed that GIRK1 and GIRK3 are the predominant GIRK subunits expressed in Prok2 neurons. Moreover, Prok2 neuron-specific deletion of GIRK3 using in vivo genome editing resulted in significant nocturnal depolarization and induced abnormalities in behavioral rhythms, including delayed activity onset and circadian period lengthening, with altered SCN network activity. Together, these findings suggest that tonic, G-protein-dependent regulation of GIRK channels provides a night-specific inhibitory mechanism that contributes to intrinsic diurnal neuronal excitability in Prok2 neurons and supports the regulation of behavioral circadian rhythms.

Animals↗
PubMed1993

Tyrosine kinase-dependent suppression of a potassium channel by the G protein-coupled m1 muscarinic acetylcholine receptor.

Neurotransmitter receptors alter membrane excitability and synaptic efficacy by generating intracellular signals that ultimately change the properties of ion channels. Through expression studies in Xenopus oocytes and mammalian cells, we found that the G protein-coupled m1 muscarinic acetylcholine receptor potently suppresses a cloned delayed rectifier K+ channel through a pathway involving phospholipase C activation and direct tyrosine phosphorylation of the K+ channel. Furthermore, analysis of neuroblastoma cells revealed that a similar tyrosine kinase-dependent pathway links endogenous G protein-coupled receptors to suppression of the native RAK channel. These results suggest a novel mechanism by which neurotransmitters and hormones may regulate a specific type of K+ channel that is widely expressed in the mammalian brain and heart.

Amino Acid Sequence↗
PubMedDate not supplied

Voltage-gated currents of rabbit A- and B-type horizontal cells in retinal monolayer cultures.

In monolayer cultures prepared from immature early postnatal rabbit retina, small populations of neurons can be demonstrated to differentiate into apparently mature A- and B-type horizontal cells. Using whole-cell, single-channel, patch-clamp recording techniques, we have analyzed the pattern of voltage-gated conductances expressed by mammalian horizontal cells under these conditions. A total of six different voltage-dependent ionic currents were recorded. Tetrodotoxin-sensitive fast sodium inward currents (INa) were found in 81% of the A-type and 90% of the B-type cells. Inward calcium currents could be demonstrated in all cells tested after blockade of other conductances. Two types of outward potassium currents with properties of the 4-aminopyridine-sensitive transient IA and the tetraethylammonium sensitive delayed rectifier IK, respectively, could be characterized in whole-cell recordings. An inward rectifying potassium current (Ianom) typical for horizontal cells was activated in response to hyperpolarizing voltage steps. These types of currents have also been described in dissociated adult horizontal cells from lower vertebrates and cat. With single-channel recordings on inside-out patches excised from B-type cells, an additional Ca(2+)-dependent current (IK(Ca)) was observed which, so far, has not been described in horizontal cells developing in situ. Our results demonstrate that cultured rabbit horizontal cells express a set of voltage-gated currents which largely, but not completely, corresponds to that described in situ for horizontal cells of other species. The culture system will allow further investigation of developmental and functional aspects of mammalian horizontal cells.

Animals↗
PubMed2006

Effect of genistein on voltage-gated potassium channels in guinea pig proximal colon smooth muscle cells.

AIM: To investigate the action of genistein (GST), a broad spectrum tyrosine kinase inhibitor, on voltage-gated potassium channels in guinea pig proximal colon smooth muscle cells. METHODS: Smooth muscle cells in guinea pig proximal colon were enzymatically isolated. Nystatin-perforated whole cell patch clamp technique was used to record potassium currents including fast transient outward current (IKto) and delayed rectifier current (IKdr), two of which were isolated pharmacologically with 10 mmol/L tetraethylammonium or 5 mmol/L 4-aminopyridine. Contamination of calcium-dependent potassium currents was minimized with no calcium and 0.2 mmol/L CdCl2 in an external solution. RESULTS: GST (10-100 micromol/L) reversibly and dose-dependently reduced the peak amplitude of IKto with an IC50 value of 22.0+/-6.9 micromol/L. To a lesser extent, IKdr was also inhibited in both peak current and sustained current. GST could not totally block the outward potassium current as a fraction of the outward potassium current, which was insensitive to GST. GST had no effect on the steady-state activation (n=6) and inactivation kinetics (n=6) of IKto. Sodium orthovanadate (1 mmol/L), a potent inhibitor of tyrosine phosphatase, significantly inhibited GST-induced inhibition (P<0.05). CONCLUSION: GST can dose-dependently and reversibly block voltage-gated potassium channels in guinea pig proximal colon smooth muscle cells.

Animals↗
PubMed1997

Developmental changes in the physiology of hair cells.

Mature hair cells express complements of ion channels which vary with hair cell type. Immature hair cells in the inner ears of neonatal mice and pre-hatch chicks share mechanosensitive and certain voltage-gated conductances: delayed rectifier and inwardly rectifying potassium conductances, voltage-gated calcium and sodium conductances. Over the course of several days the immature cells acquire other conductances that confer upon them the distinctive voltage-dependent properties of mature hair cells. In the mouse utricle, postnatal acquisition of additional delayed and inward rectifiers transforms the neonatal hair cells into two classes with the electrophysiological profiles of mature type I and type hair II cells. Electromotility, a highly differentiated, voltage-dependent property of mature outer hair cells from the mammalian cochlea, is also acquired after mechanosensitivity.

Journal Article↗
PubMed1991

Electrophysiological effects of CD-349, a dihydropyridine-type calcium antagonist, on goat cardiac Purkinje fibers.

We examined the calcium antagonistic action of CD-349, a dihydropyridine derivative, on goat cardiac Purkinje fibers using the two-microelectrode voltage-clamp method. CD-349 at a concentration of 10(-5) M shortened the action potential duration without changing the maximum rise in the action potential (Vmax) in goat Purkinje fibers. CD-349 at 3 x 10(-7) to 3 x 10(-6) M inhibited the slow inward current (Isi) in a concentration-dependent manner. At the holding potential of -55 mV, CD-349 exerted a tonic block of Isi, and, furthermore, it exerted a use-dependent block at a frequency range of 1 Hz, but it did not exert a use-dependent block at 0.5 and 0.2 Hz. This may be because CD-349 delayed the recovery process from the inactivation of Isi. The amplitude of the block of Isi was larger at the holding potential of -45 mV than at -55 mV. The inactivation curve of Isi shifted toward a negative potential in the presence of CD-349. Nifedipine also exerted a tonic block of Isi. The onset of the action of nifedipine was quicker than that of CD-349 or nitrendipine. A use-dependent block at 1 Hz and delay of the recovery process from inactivation was also observed with nifedipine. The inactivation curve shifted toward the negative potential with nifedipine. On washout of the drugs, the effects of CD-349 or nitrendipine were not readily reversed compared with those of nifedipine. CD-349 had no effect on either inward rectifying (IK1) or delayed outward potassium (IK) or hyperpolarization-activated inward (If) currents. These observations suggest that, in cardiac tissues, CD-349 selectively inhibits the calcium current, presumably by acting on the inactivated channel.

Action Potentials↗
PubMed1998

Anoxia differentially modulates multiple K+ currents and depolarizes neonatal rat adrenal chromaffin cells.

1. Using perforated-patch, whole cell recording, we investigated the membrane mechanisms underlying O2 chemosensitivity in neonatal rat adrenomedullary chromaffin cells (AMC) bathed in extracellular solution containing tetrodotoxin (TTX; 0.5-1 microM), with or without blockers of calcium entry. 2. Under voltage clamp, low PO2 (0-15 mmHg) caused a graded and reversible suppression in macroscopic outward K+ current. The suppression during anoxia (PO2 = 0 mmHg) was approximately 35% (voltage step from -60 to +30 mV) and was due to a combination of several factors: (i) suppression of a cadmium-sensitive, Ca2+-dependent K+ current, IK(CaO2); (ii) suppression of a Ca2+-insensitive, delayed rectifier type K+ current, IK(VO2); (iii) activation of a glibenclamide- (and Ca2+)-sensitive current, IK(ATP). 3. During normoxia (PO2 = 150 mmHg), application of pinacidil (100 microM), an ATP-sensitive potassium channel (KATP) activator, increased outward current density by 45.0 +/- 7.0 pA pF-1 (step from -60 to + 30 mV), whereas the KATP blocker glibenclamide (50 microM) caused only a small suppression by 6.3 +/- 4.0 pA pF-1. In contrast, during anoxia the presence of glibenclamide resulted in a substantial reduction in outward current density by 24.9 +/- 7.9 pA pF-1, which far exceeded that seen in its absence. Thus, activation of IK(ATP) by anoxia appears to reduce the overall K+ current suppression attributable to the combined effects of IK(CaO2) and IK(VO2). 4. Pharmacological tests revealed that IK(CaO2) was carried predominantly by maxi-K+ or BK potassium channels, sensitive to 50-100 nM iberiotoxin; this current also accounted for the major portion (approximately 60%) of the anoxic suppression of outward current. Tetraethylammonium (TEA; 10-20 mM) blocked all of the anoxia-sensitive K+ currents recorded under voltage clamp, i.e. IK(CaO2), IK(VO2) and IK(ATP). 5. Under current clamp, anoxia depolarized neonatal AMC by 10-15 mV from a resting potential of approximately -55 mV. At least part of this depolarization persisted in the presence of either TEA, Cd2+, 4-aminopyridine or charybdotoxin, suggesting the presence of anoxia-sensitive mechanisms additionalto those revealed under voltage clamp. In Na+/Ca2+-free solutions, the membrane hyperpolarized, though at least a portion of the anoxia-induced depolarization persisted. 6. In the presence of glibenclamide, the anoxia-induced depolarization increased significantly to approximately 25 mV, suggesting that activation of KATP channels may function to attenuate the anoxia-induced depolarization or receptor potential.

Animals↗
PubMed2002

Modulation of Kv1.5 currents by protein kinase A, tyrosine kinase, and protein tyrosine phosphatase requires an intact cytoskeleton.

The regulation of cardiac delayed rectifier potassium (Kv) currents by cAMP-dependent protein kinase (PKA) contributes to the control of blood pressure and heart rate. We investigated the modulation by PKA and protein phosphatases of cloned Kv1.5 channels expressed in Xenopus laevis oocytes. Exposure of oocytes to activators of PKA (100 nM forskolin, 1 mM 8-bromo-cAMP, or 1 mM 3-isobutyl-1-methylxanthine) had no effect on the amplitude of Kv1.5 currents. Inhibition of PKA by injection of protein kinase A inhibitor peptide or exposure to myristoylated protein kinase A inhibitor peptide (M-PKI; 100 nM) reduced currents mediated by Kv1.5. M-PKI also reduced the amplitude of currents mediated by mutated Kv1.5 channels in which the COOH terminal PKA phosphorylation sites and PSD-95, Disc-large, and ZO-1-binding domain were removed. The reduction of Kv1.5 currents by M-PKI was attenuated by inhibition of actin polymerization by 1 microM cytochalasins B and D, but was not affected by 10 microM phalloidin (stabilizes actin filaments) or 50 microM colchicine (disrupts microtubules). Treatment of oocytes with antisense oligonucleotides against alpha-actinin-2 abolished the reduction in Kv1.5 current by M-PKI. These observations suggest that Kv1.5 currents are activated by endogenous PKA in "resting" oocytes and that inhibition of PKA activity reveals the action of endogenous phosphatases. Indeed, injection of alkaline phosphatase reduced currents mediated by Kv1.5. Further preincubation of oocytes with 1 mM sodium orthovanadate (a protein tyrosine phosphatase inhibitor) abolished the reduction in Kv1.5 currents by M-PKI. We conclude that currents encoded by Kv1.5 are regulated by PKA and protein tyrosine phosphatase and that this regulation requires an intact actin cytoskeleton and alpha-actinin-2.

Actinin↗
PubMed1999

Unmasking of a novel potassium current in Drosophila by a mutation and drugs.

The delayed rectifier potassium current plays a critical role in cellular physiology. This current (I(K)) in Drosophila larvae is believed to be a single current. However, a likely null mutation in the Shab K(+) channel gene (Shab(3)) reduces I(K) but does not eliminate it. This raises a question as to whether or not the entire I(K) passes through channels encoded by one gene. Similarly, an incomplete blockade of I(K) by high concentrations of quinidine, a selective I(K) blocker, raises a question as to whether I(K) consists of two components that are differentially sensitive to quinidine. We have addressed these questions by a combined use of genetics, pharmacology, and physiology. The current component removed by the Shab(3) mutation differed from the remaining component in activation kinetics, inactivation kinetics, threshold of activation, and voltage dependence. The two components showed strong differences in sensitivity to quinidine. Physiological properties of the current component removed by the Shab(3) mutation were similar to those of the quinidine-sensitive fraction of I(K). Complementary to this, properties of the current component remaining in the Shab(3) mutant muscles were similar to those of the quinidine-resistant fraction of I(K). These observations strongly suggest that, in contrast to the current belief, I(K) consists of two components in Drosophila, which are genetically, pharmacologically, and physiologically distinct. These components are being called I(KS) and I(KF). I(KS) is carried via Shab-encoded channels. I(KF) defines a new voltage-activated K(+) current in Drosophila.

4-Aminopyridine↗
PubMed2003

Molecular variants of KCNQ channels expressed in murine portal vein myocytes: a role in delayed rectifier current.

We have analyzed the expression of KCNQ genes in murine portal vein myocytes and determined that of the 5 known KCNQ channels, only KCNQ1 was expressed. In addition to the full-length KCNQ1 transcript, a novel spliced form (termed KCNQ1b) was detected that had a 63 amino acid truncation at the C-terminus. KCNQ1b was not detected in heart or brain but represented approximately half the KCNQ1 transcripts expressed in PV. Antibodies specific for KCNQ1a stained cell membranes from portal vein myocytes and HEK cells expressing the channel. However, because the antibodies were generated against an epitope in the deleted, C-terminal portion of the protein, these antibodies did not stain HEK cells expressing KCNQ1b. In murine portal vein myocytes, in the presence of 5 mmol/L 4-aminopyridine, an outwardly rectifying K+ current was recorded that was sensitive to linopirdine, a specific blocker of KCNQ channels. Currents produced by the heterologous expression of KCNQ1a or KCNQ1b were inhibited by similar concentrations of linopirdine, and linopirdine prolonged the time-course of the action potential in isolated portal vein myocytes. Our data suggest that these two KCNQ1 splice forms are expressed in murine portal vein and contribute to the delayed rectifier current in these myocytes.

Alternative Splicing↗
PubMed1996

[Developmental changes in the pacemaker current and membrane currents of the guinea pig myocardium].

The pacemaker current (I(f)) in embryonic chick ventricular myocytes is present, but decreases during development. beta-Adrenergic agonists stimulate I(f), whereas muscarinic cholinergic agonists inhibit I(f) and reverse beta-adrenoceptor stimulation. G-proteins directly and indirectly couple autonomic receptors to I(f) channels in embryonic ventricular cells. The I(f) may contribute partly to the electrogenesis of the pacemaker potential. On the other hand, Ito current, voltage-dependent and 4-AP-sensitive, exists even in young embryonic cardiomyocytes, but not in all cells. The Ito increases during development, resulting in modulation of the action potential configuration. The action potential duration of guinea pig ventricular myocardium decreases during the late fetal period and increases postnatally. Single cell voltage clamp analyses revealed that the decrease and increase in action potential duration are due to developmental increases in the current densities of the calcium current and delayed rectifier potassium current, respectively. The role of the sarcoplasmic reticulum in contraction and relaxation of the guinea pig myocardium increases during fetal development.

Action Potentials↗
PubMed1989

Characterization of single non-inactivating potassium channels in primary neuronal cultures of Drosophila.

Permeability and gating properties of single, non-inactivating, K+ channel currents in cultured Drosophila neurons were studied using the gigaohm-seal patch-clamp technique. The non-inactivating K+ currents were activated by depolarizing the membrane to -30 mV or to more positive potentials. The slope conductance of the channel was estimated to be 17.6 +/- 3.70 pS when the cytoplasmic side of the inside-out membrane patch was perfused with solutions containing 145 mmoll-1 K+. The single-channel conductance was temperature-sensitive, with a Q10 of 1.44 between 10 and 20 degrees C. Single-channel currents could be recorded when the cytoplasmic K+ was replaced with NH4+, Rb+ or Na+, but not with Cs+. The conductance ratio of the channel for these cations was: K+ (1) greater than NH4+(0.53) greater than Rb+ (0.47) greater than Na+ (0.44). Tetraethylammonium (TEA+) ions applied at a concentration of 10 mmoll-1 to the cytoplasmic side of the membrane increased the frequency of 'blank' traces which contained no channel openings during repetitive depolarization. In addition, single-channel amplitude was reduced by about 20%. The open-time distribution was fitted by a single exponential function, whereas the closed-time distribution required a three-exponential fit. Permeability and gating properties of single, non-inactivating K+ channel currents in neurons of eag, a mutant which has defects in the delayed rectifier K+ channel, were indistinguishable from those recorded from wild-type neurons.

Action Potentials↗
PubMed1993

Plasmalemmal, voltage-dependent ionic currents from excitable pulvinar motor cells of Mimosa pudica.

Plasmalemmal ionic currents from excitable motor cells of the primary pulvinus of Mimosa pudica were investigated by patch-clamp techniques. In almost all of the enzymatically isolated protoplasts, a delayed rectifier potassium current was activated by depolarization, while no currents were detected upon hyperpolarization. This sustained outward current was reversibly blocked by Ba and TEA and serves to repolarize the membrane potential. Outward single channel currents that very likely underly the macroscopic outward potassium current had an elementary conductance of approximately 20 pS. In addition, in a few protoplasts held at hyperpolarized potentials, depolarization-activated transient inward currents were observed, and under current clamp, action potential-like responses were triggered by depolarizing current injections or by mechanical perturbations. The activation characteristics of both inward currents and spikes showed striking similarities compared to those of action potentials in situ.

Barium↗