A possible role of inwardly rectifying K+ channels in chick myoblast differentiation

1997 ◽  
Vol 272 (3) ◽  
pp. C894-C900 ◽  
Author(s):  
K. S. Shin ◽  
J. Y. Park ◽  
H. Kwon ◽  
C. H. Chung ◽  
M. S. Kang
Keyword(s):  
Time Course ◽  
Developmental Change ◽  
Myoblast Differentiation ◽  
Resting Membrane Potential ◽  
K Channels ◽  
K Concentration ◽  
Inwardly Rectifying ◽  
K Permeability ◽  
K Currents

We examined the developmental change of inwardly rectifying K+ channels (IRK) and its possible role in myogenesis. Northern blot analysis revealed an increase in the level of IRK mRNA during myogenesis. Accordingly, IRK current was not detectable in replicating myoblasts but first appeared in aligned myoblasts that were competent for fusion and gradually increased thereafter. The time course change of IRK activity was closely related to the increase in resting membrane potential during myogenesis. Application of 0.5 mM Ba2+ to the bath depolarized the membrane and blocked IRK currents dramatically but not outwardly rectifying K+ currents. Myoblasts devoid of IRK had low resting K+ permeability, whereas myotubes that possess IRK had high resting K+ permeability. In some aligned myoblasts, anomalous hyperpolarization was elicited by increasing extracellular K+ concentration, which may be attributable to the increased conductance of IRK. Noteworthy was the fact that maximal fusion was obtained at this range of K+ concentration. These findings imply that IRK is responsible for the change in the K+ permeability during chick myogenesis, which may provide a larger driving force for Ca2+ influx that is a prerequisite for myoblast fusion.

scholarly journals Kcnj16 (Kir5.1) Gene Ablation Causes Subfertility and Increases the Prevalence of Morphologically Abnormal Spermatozoa

2021 ◽  
Vol 22 (11) ◽  
pp. 5972
Author(s):  
Giulia Poli ◽  
Sonia Hasan ◽  
Silvia Belia ◽  
Marta Cenciarini ◽  
Stephen J. Tucker ◽  
...  
Keyword(s):  
High Sensitivity ◽  
Knock Out ◽  
Gene Ablation ◽  
Kir Channel ◽  
K Concentration ◽  
Knock Out Mice ◽  
Inwardly Rectifying ◽  
Dependent Processes ◽  
K Permeability

The ability of spermatozoa to swim towards an oocyte and fertilize it depends on precise K+ permeability changes. Kir5.1 is an inwardly-rectifying potassium (Kir) channel with high sensitivity to intracellular H+ (pHi) and extracellular K+ concentration [K+]o, and hence provides a link between pHi and [K+]o changes and membrane potential. The intrinsic pHi sensitivity of Kir5.1 suggests a possible role for this channel in the pHi-dependent processes that take place during fertilization. However, despite the localization of Kir5.1 in murine spermatozoa, and its increased expression with age and sexual maturity, the role of the channel in sperm morphology, maturity, motility, and fertility is unknown. Here, we confirmed the presence of Kir5.1 in spermatozoa and showed strong expression of Kir4.1 channels in smooth muscle and epithelial cells lining the epididymal ducts. In contrast, Kir4.2 expression was not detected in testes. To examine the possible role of Kir5.1 in sperm physiology, we bred mice with a deletion of the Kcnj16 (Kir5.1) gene and observed that 20% of Kir5.1 knock-out male mice were infertile. Furthermore, 50% of knock-out mice older than 3 months were unable to breed. By contrast, 100% of wild-type (WT) mice were fertile. The genetic inactivation of Kcnj16 also resulted in smaller testes and a greater percentage of sperm with folded flagellum compared to WT littermates. Nevertheless, the abnormal sperm from mutant animals displayed increased progressive motility. Thus, ablation of the Kcnj16 gene identifies Kir5.1 channel as an important element contributing to testis development, sperm flagellar morphology, motility, and fertility. These findings are potentially relevant to the understanding of the complex pHi- and [K+]o-dependent interplay between different sperm ion channels, and provide insight into their role in fertilization and infertility.

Hyperpolarizing effect of aminophylline, theophylline, and cAMP on rat diaphragm fibers

1988 ◽  
Vol 64 (5) ◽  
pp. 1893-1899 ◽  
Author(s):  
O. Delbono ◽  
B. A. Kotsias
Keyword(s):  
Normal Values ◽  
Bath Temperature ◽  
Resting Membrane Potential ◽  
Maximum Effect ◽  
Dependent Manner ◽  
Rat Diaphragm ◽  
K Concentration ◽  
Dose Dependent ◽  
K Permeability

We studied the effect of aminophylline and theophylline (0.1–2 mM) on the resting membrane potential (Vm) of rat diaphragm fibers in vitro (25 degrees C). The main findings are the following. 1) Aminophylline and theophylline hyperpolarize the fibers in a dose-dependent manner. This effect is present with 0.1 and 0.25 mM of aminophylline and theophylline, respectively, and the maximum effect is reached with 1 mM of the drug (approximately 5–8 mV in comparison to the normal values). This effect is reversible by washing out the preparation with normal solution. 2) Dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP, 2 mM) produces a similar increment in the Vm. 3) The hyperpolarizing action observed in the presence of aminophylline, theophylline, and DBcAMP is suppressed by 5 X 10(-4) M ouabain or by lowering the bath temperature to 5 degrees C. These results suggest that the xanthines may directly or indirectly stimulate a Na-K pump. Two possibilities may be considered: 1) an electrogenic effect of the Na-K pump and 2) a reduction in the extracellular K+ concentration in the solution contacting the external side of the cell as a consequence of the activity of the Na-K pump. Alternative mechanisms such as a reduction in Na permeability or an increment in K permeability might collaborate in the hyperpolarizing effect of the drugs tested.

Stimulation of prolactin release by dopamine withdrawal: role of membrane hyperpolarization

1994 ◽  
Vol 267 (5) ◽  
pp. E781-E788 ◽  
Author(s):  
K. A. Gregerson ◽  
N. Golesorkhi ◽  
R. Chuknyiska
Keyword(s):  
Resting Membrane Potential ◽  
Prolactin Release ◽  
Membrane Hyperpolarization ◽  
Basal Release ◽  
K Concentration ◽  
Hypothalamic Dopamine ◽  
Ca2 Channels ◽  
Stimulation Of ◽  
External K

Hypothalamic dopamine (DA) tonically inhibits prolactin (PRL) release from the anterior pituitary gland, whereas removal of DA markedly augments its release to values exceeding pre-DA rates. We investigated whether electrical events induced by DA contribute to this secretory rebound. In primary cultured lactotropes, spontaneous Ca(2+)-dependent spiking activity was enhanced after recovery from DA-induced hyperpolarization. Voltage clamp studies showed a rapidly and a slowly inactivating Ca2+ current that were both augmented by a hyperpolarizing conditioning potential. We measured PRL release from perifused cells exposed to DA to correlate the electrical with the secretory responses. DA inhibited PRL release by 67%, whereas PRL secretion increased three- to fourfold over basal release after washout of DA. Valinomycin, used to directly hyperpolarize the cell membrane, mimicked the actions of DA, inhibiting PRL release (65%) and, upon washout, augmenting PRL secretion. Blocking the DA- or valinomycin-induced hyperpolarization by elevating external K+ concentration blocked both the inhibition and rebound of PRL release. These novel results demonstrate that hyperpolarization of the lactotrope membrane by DA is critical for the development of PRL rebound after DA withdrawal. We hypothesize the mechanism involves the removal of inactivation from a population of Ca2+ channels, leading to enhanced Ca2+ influx and PRL release upon recovery of the resting membrane potential after DA removal.

Eicosanoids modulate apical Ca(2+)-dependent K+ channels in cultured rabbit principal cells

1992 ◽  
Vol 263 (1) ◽  
pp. F116-F126 ◽  
Author(s):  
B. N. Ling ◽  
C. L. Webster ◽  
D. C. Eaton
Keyword(s):  
Single Channel ◽  
Primary Cultures ◽  
Cell Volume Regulation ◽  
Principal Cell ◽  
Resting Membrane Potential ◽  
Open Probability ◽  
Channel Activation ◽  
K Channels ◽  
Pg E2

Patch clamp technology was utilized to study the effects of apical phospholipase A2 (PLA2) metabolites on “maxi K” channels in the principal cell apical membrane of rabbit cortical collecting tubule (CCT) primary cultures (B. N. Ling, C. F. Hinton, and D. C. Eaton. Kidney Int. 40: 441–452, 1991). At resting membrane potential, this channel is quiescent in the cell-attached configuration. Apical application of the PLA2 agonist melittin (1 microgram/ml) for 10 min increased single-channel open probability (Po) from 0.0004 +/- 0.0010 to 0.11 +/- 0.05. Similarly, apical exposure to 50 microM arachidonic acid (AA) or 0.5 microM prostaglandin (PG) E2, but not 0.5 microM PGF2 alpha, also increased channel activity. Conversely, 10 microM of the PLA2 antagonist quinacrine applied apically decreased Po. Removal of apical bath Ca2+ did not prevent melittin-, AA-, or PGE2-induced channel activation. We then examined the role of maxi K channels and eicosanoids in principal cell volume regulation. Within seconds of reducing basolateral bath tonicity (285 to 214 mosmol/kgH2O), NPo (i.e., no. of channels x Po) initially increased approximately 200%, followed by a delayed but prolonged activation phase that was attenuated by removal of apical bath Ca2+. Pretreatment with 10 microM quinacrine, 100 microM indomethacin (cyclooxygenase inhibitor), or 0.25 microM thapsigargin (to deplete intracellular Ca2+ stores) abolished the initial phase of swelling-induced channel activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic hypoxia alters effects of endothelin and angiotensin on K+ currents in pulmonary arterial myocytes

1999 ◽  
Vol 277 (3) ◽  
pp. L431-L439 ◽  
Author(s):  
Larissa A. Shimoda ◽  
J. T. Sylvester ◽  
James S. K. Sham
Keyword(s):  
Smooth Muscle ◽  
Chronic Hypoxia ◽  
Inhibitory Effect ◽  
Resting Membrane Potential ◽  
Ang Ii ◽  
Voltage Gated ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells ◽  
K Currents

We tested the hypothesis that chronic hypoxia alters the regulation of K+ channels in intrapulmonary arterial smooth muscle cells (PASMCs). Charybdotoxin-insensitive, 4-aminopyridine-sensitive voltage-gated K+(KV,CI) and Ca2+-activated K+(KCa) currents were measured in freshly isolated PASMCs from rats exposed to 21 or 10% O2 for 17–21 days. In chronically hypoxic PASMCs, KV,CIcurrent was reduced and KCacurrent was enhanced. 4-Aminopyridine (10 mM) depolarized both normoxic and chronically hypoxic PASMCs, whereas charybdotoxin (100 nM) had no effect in either group. The inhibitory effect of endothelin (ET)-1 (10−7 M) on KV,CI current was significantly reduced in PASMCs from chronically hypoxic rats, whereas inhibition by angiotensin (ANG) II (10−7M) was enhanced. Neither ET-1 nor ANG II altered KCa current in normoxic PASMCs; however, both stimulated KCacurrent at positive potentials in chronically hypoxic PASMCs. These results suggest that although modulation of KV,CI and KCa channels by ET-1 and ANG II is altered by chronic hypoxia, the role of these channels in the regulation of resting membrane potential was not changed.

5-HT modulation of hyperpolarization-activated inward current and calcium-dependent outward current in a crustacean motor neuron

1992 ◽  
Vol 68 (2) ◽  
pp. 496-508 ◽  
Author(s):  
O. Kiehn ◽  
R. M. Harris-Warrick
Keyword(s):  
Motor Neuron ◽  
Time Course ◽  
Reversal Potential ◽  
Outward Current ◽  
Resting Membrane Potential ◽  
Inward Current ◽  
Calcium Dependent ◽  
Voltage Dependent ◽  
K Concentration ◽  
Conductance Increase

1. Serotonergic modulation of a hyperpolarization-activated inward current, Ih, and a calcium-dependent outward current, Io(Ca), was examined in the dorsal gastric (DG) motor neuron, with the use of intracellular recording techniques in an isolated preparation of the crab stomatogastric ganglion (STG). 2. Hyperpolarization of the membrane from rest with maintained current pulses resulted in a slow time-dependent relaxation back toward rest and a depolarizing overshoot after termination of the current pulse. In voltage clamp, hyperpolarizing commands negative to approximately -70 mV caused a slowly developing inward current, Ih, which showed no inactivation. Repolarization back to the holding potential of -50 mV revealed a slow inward tail current. 3. The reversal potential for Ih was approximately -35 mV. Raising extracellular K+ concentration ([K+]o) from 11 to 22 mM enhanced, whereas decreasing extracellular Na+ concentration ([Na+]o) reduced the amplitude of Ih. These results indicate that Ih in DG is carried by both K+ and Na+ ions. 4. Bath application of serotonin (5-HT; 10 microM) caused a marked increase in the amplitude of Ih through its active voltage ranges. 5. The time course of activation of Ih was well fitted by a single exponential function and strongly voltage dependent. 5-HT increased the rate of activation of Ih. 5-HT also slowed the rate of deactivation of the Ih tail on repolarization to -50 mV. 6. The activation curve for the conductance (Gh) underlying Ih was obtained by analyzing tail currents. 5-HT shifted the half activation for Gh from approximately -105 mV in control to -95 mV, resulting in an increase in the amplitude of Gh active at rest. 7. Two to 4 mM Cs+ abolished Ih, whereas barium (200 microM to 2 mM) had only weak suppressing effects on Ih. Concomitantly, Cs+ also blocked the 5-HT-induced inward current and conductance increase seen at voltages negative to rest. In current clamp, Cs+ caused DG to hyperpolarize 3-4 mV from rest, suggesting that Ih is partially active at rest and contributes to the resting membrane potential. 8. Depolarizing voltage commands from a holding potential of -50 mV resulted in a total outward current (Io) with an initial transient component and a sustained steady-state component. Application of 5-HT reduced both the transient and sustained components of Io. 9. Io was reduced by 10-20 mM tetraethylammonium (TEA), suggesting that it is primarily a K+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Molecular Background of Leak K+ Currents: Two-Pore Domain Potassium Channels

2010 ◽  
Vol 90 (2) ◽  
pp. 559-605 ◽  
Author(s):  
Péter Enyedi ◽  
Gábor Czirják
Keyword(s):  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Detailed Examination ◽  
Resting Membrane Potential ◽  
Membrane Stretch ◽  
Physiological Processes ◽  
Pore Domain ◽  
K Currents

Two-pore domain K+ (K2P) channels give rise to leak (also called background) K+ currents. The well-known role of background K+ currents is to stabilize the negative resting membrane potential and counterbalance depolarization. However, it has become apparent in the past decade (during the detailed examination of the cloned and corresponding native K2P channel types) that this primary hyperpolarizing action is not performed passively. The K2P channels are regulated by a wide variety of voltage-independent factors. Basic physicochemical parameters (e.g., pH, temperature, membrane stretch) and also several intracellular signaling pathways substantially and specifically modulate the different members of the six K2P channel subfamilies (TWIK, TREK, TASK, TALK, THIK, and TRESK). The deep implication in diverse physiological processes, the circumscribed expression pattern of the different channels, and the interesting pharmacological profile brought the K2P channel family into the spotlight. In this review, we focus on the physiological roles of K2P channels in the most extensively investigated cell types, with special emphasis on the molecular mechanisms of channel regulation.

K+ channels in adrenal zona glomerulosa cells. I. Characterization of distinct channel types

1992 ◽  
Vol 263 (4) ◽  
pp. E752-E759 ◽  
Author(s):  
P. M. Vassilev ◽  
M. V. Kanazirska ◽  
S. J. Quinn ◽  
D. L. Tillotson ◽  
G. H. Williams
Keyword(s):  
Single Channel ◽  
Zona Glomerulosa ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
K Channels ◽  
Outward Currents ◽  
Positive Voltage ◽  
K Concentration ◽  
Inward Rectifier Channels

Four distinct types of K+ channels were identified in rat and bovine adrenal zona glomerulosa (ZG) cells and characterized using single-channel recording techniques. Inward rectifier channels were the most frequently observed K+ channel types in the membrane patches of both rat and bovine ZG cells. The slope conductance of the inward current was 42 pS with an extracellular K+ concentration of 150 mM. The probability of the open state of these channels increased with depolarization. With the use of inside-out membrane patches with symmetric 150 mM K+ solutions, the rectifying behavior was found to require Mg2+ on the intracellular side of the membrane. Delayed rectifier K+ channels with conductances of 27 and 48 pS were found with rat ZG cells. These channels persisted with prolonged positive voltage steps and showed long mean open times with increasing depolarization. Transient outward currents with a conductance of 28 pS were observed only in bovine ZG cells. These channels showed substantial inactivation during positive voltage steps of 250 ms duration. Ca(2+)-activated K+ channels with a large conductance (228 pS) were identified in rat and bovine ZG cells. These different classes of K+ channels may be important for the control of resting membrane potential and the generation of action potentials, thus participating in the regulation of Ca2+ influx and aldosterone secretion in ZG cells.

scholarly journals Increased ACh-Associated Immunoreactivity in Autonomic Centers in PTZ Kindling Model of Epilepsy

Biomedicines ◽  
2020 ◽  
Vol 8 (5) ◽  
pp. 113 ◽  
Author(s):  
Enes Akyüz ◽  
Züleyha Doğanyiğit ◽  
Yam Nath Paudel ◽  
Emin Kaymak ◽  
Seher Yilmaz ◽  
...  
Keyword(s):  
Ion Channel ◽  
Resting Membrane Potential ◽  
Cardiac Pathology ◽  
Kindling Model ◽  
Cell Excitability ◽  
Ptz Kindling ◽  
Targeted Expression ◽  
Inwardly Rectifying ◽  
Histological Staining

Experimental and clinical studies of cardiac pathology associated with epilepsy have demonstrated an impact on the autonomic nervous system (ANS). However, the underlying molecular mechanism has not been fully elucidated. Molecular investigation of the neurotransmitters related receptor and ion channel directing ANS might help in understanding the associated mechanism. In this paper, we investigated the role of acetylcholine (ACh), which demonstrates both sympathetic and parasympathetic roles in targeted expression in terms of the relevant receptor and ion channel. Inwardly rectifying potassium (Kir) channels play a significant role in maintaining the resting membrane potential and controlling cell excitability and are prominently expressed in both the excitable and non-excitable tissues. The immunoreactivity of ACh-activated Kir3.1 channel and muscarinic ACh receptors (M2) in autonomic centers such as the brainstem, vagus nerve (VN) and atria of heart was confirmed by both histological staining and pathological tissue analysis. Significant upregulations of Kir3.1 and M2 receptors were observed in pentylenetetrazol (PTZ)-kindled epileptic rats for all related tissues investigated, whereas no pathological difference was observed. These findings provide proof-of-concept that changes in ACh-associated immunoreactivity might be linked to the ANS dysfunctions associated with epilepsy.

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