The sea anemone toxin AdE-1 modifies both sodium and potassium currents of rat cardiomyocytes

2014 ◽  
Vol 461 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Nir Nesher ◽  
Eliahu Zlotkin ◽  
Binyamin Hochner
Keyword(s):  
Potassium Currents ◽  
Sea Anemone ◽  
Na Current ◽  
Rat Cardiomyocytes ◽  
K Current ◽  
Sea Anemone Toxin ◽  
Sodium And Potassium ◽  
K Currents

AdE-1 modifies both Na+ and K+ currents in rat cardiomyocytes. Although the effects on the Na+ current are not exclusively different from other anemone toxins, its additional effect on the K+ current is a novel phenomenon which has not yet been reported.

Potential-dependent block of human delayed rectifier K+ channels by internal Na+

1996 ◽  
Vol 270 (4) ◽  
pp. C1131-C1144 ◽  
Author(s):  
S. Johansson ◽  
A. K. Sundgren ◽  
U. Kahl
Keyword(s):  
Single Channel ◽  
Neuroblastoma Cells ◽  
Negative Slope ◽  
Delayed Rectifier ◽  
Na Current ◽  
Intact Cells ◽  
K Channels ◽  
High Potentials ◽  
K Current ◽  
K Currents

The delayed rectifier K+ currents in differentiated human SH-SY5Y neuroblastoma cells were characterized with tight-seal recording techniques. Activation and inactivation parameters were measured. At high positive potentials, the current showed a marked rectification, causing a region of negative slope conductance in the current vs. potential curve. The rectification depended markedly on the pipette Na+ concentration. Without Na+, no rectification was observed, whereas with high Na+ (20-60 mM), a marked rectification was always observed. Tail current measurements showed a fast ( < 400 microseconds) block of K+ currents in the presence of internal Na+. With 60 mM Na+ in the pipette 8% of the K+ current was blocked at 0 mV, 27% at +20 mV, and 82% at +100 mV. Similar degrees of block were often seen with 30 mM Na+ in the pipette. The submembrane Na+ concentration in intact cells was estimated, on the basis of the reversal of Na+ current, to be approximately 15 mM. Single-channel K+ currents, in the cell-attached configuration, showed a conductance of approximately 20 pS at 40-60 mV above rest but showed rectification at high potentials.

scholarly journals Ionic currents and ion channels of lobster olfactory receptor neurons.

1989 ◽  
Vol 94 (6) ◽  
pp. 1085-1099 ◽  
Author(s):  
T S McClintock ◽  
B W Ache
Keyword(s):  
Ion Channels ◽  
Olfactory Receptor ◽  
Ionic Currents ◽  
K Channel ◽  
Delayed Rectifier ◽  
Na Current ◽  
Cl Channel ◽  
Inward Currents ◽  
K Current ◽  
K Currents

The role of the soma of spiny lobster olfactory receptor cells in generating odor-evoked electrical signals was investigated by studying the ion channels and macroscopic currents of the soma. Four ionic currents; a tetrodotoxin-sensitive Na+ current, a Ca++ current, a Ca(++)-activated K+ current, and a delayed rectifier K+ current, were isolated by application of specific blocking agents. The Na+ and Ca++ currents began to activate at -40 to -30 mV, while the K+ currents began to activate at -30 to -20 mV. The size of the Na+ current was related to the presence of a remnant of a neurite, presumably an axon, and not to the size of the soma. No voltage-dependent inward currents were observed at potentials below those activating the Na+ current, suggesting that receptor potentials spread passively through the soma to generate action potentials in the axon of this cell. Steady-state inactivation of the Na+ current was half-maximal at -40 mV. Recovery from inactivation was a single exponential function that was half-maximal at 1.7 ms at room temperature. The K+ currents were much larger than the inward currents and probably underlie the outward rectification observed in this cell. The delayed rectifier K+ current was reduced by GTP-gamma-S and AIF-4, agents which activate GTP-binding proteins. The channels described were a 215-pS Ca(++)-activated K+ channel, a 9.7-pS delayed rectifier K+ channel, and a 35-pS voltage-independent Cl- channel. The Cl- channel provides a constant leak conductance that may be important in stabilizing the membrane potential of the cell.

scholarly journals The Electrophysiology of Cnidocytes

1987 ◽  
Vol 133 (1) ◽  
pp. 215-230 ◽  
Author(s):  
PETER A. V. ANDERSON ◽  
M. CRAIG MCKAY
Keyword(s):  
Action Potentials ◽  
Ionic Currents ◽  
Na Current ◽  
Selective Blockade ◽  
Current Voltage ◽  
Inward Currents ◽  
K Current ◽  
A Current ◽  
K Currents

Electrical properties of cnidocytes isolated from the hydroid Cladonema and the scyphomedusa Chrysaora were examined using current- and voltage-clamp recording techniques. The stenoteles of Cladonema produced action potentials when depolarized above 0 m V. The inward current that produced the action potential was a Na+ current. These cells also possessed an A-current and a K-current. Atrichous isorhizas from Chrysaora did not spike and did not have any inward currents. All cells examined had K-currents, some had A-currents also. Very few cnidocytes discharged during the course of the recordings, irrespective of the degree to which they were depolarized or hyperpolarized, or the presence or selective blockade of any ionic currents. When discharge did occur it could never be correlated with any obvious electrophysiological event. Recordings from cnidocytes in situ in tentacles of the siphonophore Physalia indicate that these cells do not spike. Their current/voltage relationships were linear. They too did not discharge in response to changes in membrane potential, suggesting that the failure of isolated cnidocytes to discharge cannot be attributed to the isolation procedure.

Characterization of voltage-sensitive Na+ and K+ currents recorded from acutely dissociated pelvic ganglion neurons of the adult rat

1996 ◽  
Vol 76 (4) ◽  
pp. 2508-2521 ◽  
Author(s):  
N. Yoshimura ◽  
W. C. De Groat
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Na Current ◽  
Bath Application ◽  
Maximal Activation ◽  
Steady State Inactivation ◽  
Slope Factor ◽  
K Current ◽  
Ia Current ◽  
K Currents

1. Electrophysiological properties of acutely dissociated neurons from the major pelvic ganglion (MPG) of the adult male rat were studied with whole cell patch-clamp recording techniques. The MPG neurons innervating the urinary bladder were labeled by retrograde axonal tracing methods with the use of a fluorescent dye, Fast Blue (FB) injected into the bladder wall and identified with a fluorescent microscope. 2. Passive and active membrane properties such as resting membrane potential, input resistance, duration of action potentials, thresholds for spike activation, or duration of afterhyperpolarization in unidentified MPG neurons were comparable with those of FB-labeled neurons innervating the urinary bladder. The action potential in both unidentified and bladder efferent MPG neurons was reversibly abolished by tetrodotoxin (TTX, 1 microM). The afterhyperpolarization of the TTX-sensitive action potential in both groups was reduced by application of Cd2+ (0.1 mM) and further suppressed by tetraethylammonium (TEA, 10 mM). Extracellularly applied TEA increased the duration of the action potential, and 4-aminopyridine (4-AP, 1 or 2 mM) also reduced the spike afterhyperpolarization and increased the spike duration. The duration of the action potential was decreased and the rate of spike repolarization was increased by approximately 2.5-fold with negative shift of membrane potential from -40 to -80 mV. 3. The isolated Na+ current was reversibly blocked by 1 microM TTX and had a mean peak amplitude of 127.3 pA/pF when activated from a holding potential of -70 mV in the external solution containing 100 mM Na+. The Na+ conductance reached half-maximal activation at a membrane potential of -21.5 mV with a slope factor of 4.9 mV. The steady-state inactivation of Na+ conductance occurred at membrane potentials more depolarized than -90 mV, and the half-maximal inactivation was obtained at -57.5 mV with a slope factor of 8.8 mV. 4. The fast-transient A-type K+ current (IA) was activated at membrane potentials more depolarized than -60 mV from a holding membrane potential of -100 mV, reached a peak amplitude within 10 ms after the onset of depolarizing voltage steps, and decayed within 20-30 ms at membrane potential depolarizations to +20 to +30 mV. The IA current activated by a voltage step to +20 mV from a holding potential of -100 mV averaged 102.1 pA/pF. The half-maximal activation of the IA conductance was obtained at a membrane potential of -21.2 mV with a slope factor of 9.9 mV. In steady-state inactivation of IA current, the half-maximal inactivation occurred at -76.5 mV and the slope factor was 8.0 mV. 5. The delayed K+ current was reduced by 25-35% by bath application of Cd2+ or the elimination of extracellular Ca2+ ions. The bath application of 4-AP (2 mM) suppressed the IA current by 75% and the delayed K+ current by 60%. Extracellularly applied TEA (10 mM) suppressed the delayed K+ current by 90%, but suppressed the IA current by only 16%. 6. These results indicate that bladder neurons and unidentified neurons in the MPG have similar properties including a TTX-sensitive Na+ current and three distinct types of voltage-sensitive K+ currents-IA current, Ca(2+)-activating K+ current, and delayed rectifier K+ current-that contribute to the repolarization phase of the action potential. These electrical properties of the MPG neurons resemble those of sympathetic neurons in the superior cervical and inferior mesenteric ganglia.

Effect of new O-superfamily conotoxin SO3 on sodium and potassium currents of cultured hippocampal neurons

2003 ◽  
Vol 965 (1-2) ◽  
pp. 155-158 ◽  
Author(s):  
Zhan Li ◽  
Xiang-Ping He ◽  
Zuo-Ping Xie ◽  
Qiu-Yun Dai ◽  
Pei-Tang Huang
Keyword(s):  
Hippocampal Neurons ◽  
Potassium Currents ◽  
Sodium And Potassium ◽  
Cultured Hippocampal Neurons

scholarly journals Gonadotropin-Releasing Hormone Inhibits Ether-à-Go-Go-Related Gene K+ Currents in Mouse Gonadotropes

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 1079-1088 ◽  
Author(s):  
Wiebke Hirdes ◽  
Crenguta Dinu ◽  
Christiane K. Bauer ◽  
Ulrich Boehm ◽  
Jürgen R. Schwarz
Keyword(s):  
Resting Potential ◽  
Related Gene ◽  
Activation Curve ◽  
Signal Cascade ◽  
Primary Mouse ◽  
Voltage Dependent ◽  
K Current ◽  
Unknown Signal ◽  
Ca2 Channels ◽  
K Currents

Secretion of LH from gonadotropes is initiated by a GnRH-induced increase in intracellular Ca2+ concentration ([Ca2+]i). This increase in [Ca2+]i is the result of Ca2+ release from intracellular stores and Ca2+ influx through voltage-dependent Ca2+ channels. Here we describe an ether-à-go-go-related gene (erg) K+ current in primary mouse gonadotropes and its possible function in the control of Ca2+ influx. To detect gonadotropes, we used a knock-in mouse strain, in which GnRH receptor-expressing cells are fluorescently labeled. Erg K+ currents were recorded in 80–90% of gonadotropes. Blockage of erg currents by E-4031 depolarized the resting potential by 5–8 mV and led to an increase in [Ca2+]i, which was abolished by nifedipine. GnRH inhibited erg currents by a reduction of the maximal erg current and in some cells additionally by a shift of the activation curve to more positive potentials. In conclusion, the erg current contributes to the maintenance of the resting potential in gonadotropes, thereby securing a low [Ca2+]i by restricting Ca2+ influx. In addition, the erg channels are modulated by GnRH by an as-yet unknown signal cascade.

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