Sexual behaviour in Euplotes raikovi is accompanied by pheromone-induced modifications of ionic currents

1999 ◽  
Vol 202 (4) ◽  
pp. 475-483
Author(s):  
C. Stock ◽  
T. Krüppel ◽  
G. Key ◽  
W. Lueken
Keyword(s):  
Mating Type ◽  
Sexual Behaviour ◽  
Walking Speed ◽  
Ionic Currents ◽  
Marine Ciliate ◽  
Na Current ◽  
Threefold Increase ◽  
The Mean ◽  
Euplotes Raikovi ◽  
K Currents

In the marine ciliate Euplotes raikovi, pheromone released by a complementary mating type (nonself pheromone) induces typical sexual behaviour, whereas self pheromone released by the same mating type generally has no effect. Nonself pheromone evokes a reduction of the mean walking speed by 66 %, a threefold increase in the frequency and duration of long-lasting rest phases and a doubling in the number of side-stepping reactions. Consequently, translocation is strongly reduced and the cells remain in a small area. This could increase the probability of finding a sexual partner for pair formation (conjugation). The usual pattern of rhythmic, spontaneous depolarizations controlling the walking rhythm is absent in nonself-pheromone-stimulated cells. The remaining depolarizations arise from a 4 mV hyperpolarized membrane potential and do not reach the usual amplitudes of 15–20 mV but only of 6–10 mV. In addition, the amplitudes of K+ currents are increased at depolarizations of more than 20 mV by at least 30 %. Hyperpolarization- and depolarization-activated Na+ current amplitudes are increased, whereas the Ca2+ current amplitude remains nearly unaffected.

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.

Abstract 17570: Rescue of Dilated Cardiomyopathy in Nav1.5 Mutant Mice Defective in Calmodulin Binding by Inhibition of Late Na+ Current

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hana Cho ◽  
Takeshi Aiba ◽  
Deborah DiSilvestre ◽  
Victoria Halperin ◽  
Eiki Takimoto ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Sodium Current ◽  
Ionic Currents ◽  
Na Channel ◽  
Binding Motif ◽  
Na Channels ◽  
Na Current ◽  
Down Regulation ◽  
K Currents

Introduction: Nav1.5, the main voltage-gated Na+ channel in the heart, has been shown to be involved in many cardiac diseases such as long QT syndrome, Brugada syndrome, and heart failure. Na+ channels are importantly regulated by Ca2+ calmodulin (CaM) mediated signaling: however, a fundamental understanding and physiological significance of CaM regulation of Na+ channel is incomplete. Here, we have created a transgenic mouse that harbors a mutated CaM binding motif (NaV1.5-IQ/AA), which is critical for Na+ channel regulation by Ca2+-CaM. Methods: Ventricle mass and function were analyzed with electrocardiogram, echocardiogram, and detailed invasive pressure-volume analysis. Additionally, single ventricular myocytes were obtained. Whole cell patch clamp was used to record membrane ionic currents, including sodium current, Ca2+ current, K+ currents and NCX current. Results: Homozygous mice are embryonic lethal and IQ/AA+/- mice exhibit a dramatic phenotype consisting of dilated cardiomyopathy (DCM) at 4-6 months of age with prolongation of QT. The Na+ current in IQ mice exhibits an enhanced slowly inactivating late component (INa,L) with concomitant up regulation of Na+/Ca2+ exchanger currents. Consistent with other models of DCM and heart failure, DCM in IQ/AA+/- mice was associated with a down regulation of transient outward K+ currents (Ito) and an increase in T-type Ca2+ currents. Chronic treatment with ranolazine designed to block INa,L prevented electrical remodeling of the hearts including an increase in INa,L and a down regulation of Ito. Consistent with the changes in INa,L and Ito, in ranolazine-fed IQ/AA+/- mice, the QT interval was decreased compared to vehicle (p<0.05). Further, the contractile dysfunction, cardiac hypertrophy, and myocardial fibrosis were attenuated in all ranolazine- fed animals, while ventricular dysfunction persisted in animals not fed drug (p<0.05). Conclusions: The data suggest that loss of CaM-mediated regulation of Na+ channel induces dilated cardiomyopathy by enhancing late Na+ current. Taken together, our data demonstrate a dynamic interplay for Ca2+ and Na+ signaling via the CaM binding motif of Na+ channels and highlight the critical importance of late Na+ currents to myopathy and arrhythmia.

Basis for tetrodotoxin and lidocaine effects on action potentials in dog ventricular myocytes

1988 ◽  
Vol 254 (6) ◽  
pp. H1157-H1166 ◽  
Author(s):  
J. A. Wasserstrom ◽  
J. J. Salata
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Ionic Currents ◽  
Detectable Effect ◽  
Na Channel ◽  
Na Current ◽  
Voltage Range ◽  
Purkinje Fibers ◽  
Ventricular Cells

We studied the effects of tetrodotoxin (TTX) and lidocaine on transmembrane action potentials and ionic currents in dog isolated ventricular myocytes. TTX (0.1-1 x 10(-5) M) and lidocaine (0.5-2 x 10(-5) M) decreased action potential duration, but only TTX decreased the maximum rate of depolarization (Vmax). Both TTX (1-2 x 10(-5) M) and lidocaine (2-5 x 10(-5) M) blocked a slowly inactivating toward current in the plateau voltage range. The voltage- and time-dependent characteristics of this current are virtually identical to those described in Purkinje fibers for the slowly inactivating inward Na+ current. In addition, TTX abolished the outward shift in net current at plateau potentials caused by lidocaine alone. Lidocaine had no detectable effect on the slow inward Ca2+ current and the inward K+ current rectifier, Ia. Our results indicate that 1) there is a slowly inactivating inward Na+ current in ventricular cells similar in time, voltage, and TTX sensitivity to that described in Purkinje fibers; 2) both TTX and lidocaine shorten ventricular action potentials by reducing this slowly inactivating Na+ current; 3) lidocaine has no additional actions on other ionic currents that contribute to its ability to abbreviate ventricular action potentials; and 4) although both agents shorten the action potential by the same mechanism, only TTX reduces Vmax. This last point suggests that TTX produces tonic block of Na+ current, whereas lidocaine may produce state-dependent Na+ channel block, namely, blockade of Na+ current only after Na+ channels have already been opened (inactivated-state block).

scholarly journals Kinetic analysis of the action of Leiurus scorpion alpha-toxin on ionic currents in myelinated nerve.

1985 ◽  
Vol 86 (5) ◽  
pp. 739-762 ◽  
Author(s):  
G K Wang ◽  
G Strichartz
Keyword(s):  
Steady State ◽  
Ionic Currents ◽  
Na Channel ◽  
Dependent Manner ◽  
Na Current ◽  
Toxin Concentration ◽  
Toxin Molecule ◽  
Channel Inactivation ◽  
Na Currents ◽  
Voltage Dependent

The effects of a neurotoxin, purified from the venom of the scorpion Leiurus quinquestriatus, on the ionic currents of toad single myelinated fibers were studied under voltage-clamp conditions. Unlike previous investigations using crude scorpion venom, purified Leiurus toxin II alpha at high concentrations (200-400 nM) did not affect the K currents, nor did it reduce the peak Na current in the early stages of treatment. The activation of the Na channel was unaffected by the toxin, the activation time course remained unchanged, and the peak Na current vs. voltage relationship was not altered. In contrast, Na channel inactivation was considerably slowed and became incomplete. As a result, a steady state Na current was maintained during prolonged depolarizations of several seconds. These steady state Na currents had a different voltage dependence from peak Na currents and appeared to result from the opening of previously inactivated Na channels. The opening kinetics of the steady state current were exponential and had rates approximately 100-fold slower than the normal activation processes described for transitions from the resting state to the open state. In addition, the dependence of the peak Na current on the potential of preceding conditioning pulses was also dramatically altered by toxin treatment; this parameter reached a minimal value near a membrane potential of -50 mV and then increased continuously to a "plateau" value at potentials greater than +50 mV. The amplitude of this plateau was dependent on toxin concentration, reaching a maximum value equal to approximately 50% of the peak current; voltage-dependent reversal of the toxin's action limits the amplitude of the plateauing effect. The measured plateau effect was half-maximum at a toxin concentration of 12 nM, a value quite similar to the concentration producing half of the maximum slowing of Na channel inactivation. The results of Hill plots for these actions suggest that one toxin molecule binds to one Na channel. Thus, the binding of a single toxin molecule probably both produces the steady state currents and slows the Na channel inactivation. We propose that Leiurus toxin inhibits the conversion of the open state to inactivated states in a voltage-dependent manner, and thereby permits a fraction of the total Na permeability to remain at membrane potentials where inactivation is normally complete.

scholarly journals Iron absorption from rice meals cooked with fortified salt containing ferrous sulphate and ascorbic acid

1974 ◽  
Vol 31 (3) ◽  
pp. 367-375 ◽  
Author(s):  
M. H. Sayers ◽  
S. R. Lynch ◽  
R. W. Charlton ◽  
T. H. Bothwell ◽  
R. B. Walker ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Iron Absorption ◽  
Ferrous Sulphate ◽  
Striking Difference ◽  
Red Cell ◽  
Indian Women ◽  
Threefold Increase ◽  
Cooking Process ◽  
Wide Range ◽  
The Mean

1. Iron absorption from rice-containing meals was measured by red cell utilization of radioactive Fe in sixty-six volunteer multiparous Indian women.2. In all the studies salt added during the cooking process was used as the carrier for supplemental inorganic Fe and ascorbic acid.3. Intrinsic Fe in the rice and supplementary inorganic Fe were absorbed to the same extent, with a wide range of absorption values.4. There was a striking difference between the mean absorption of a 3 mg dose of ferrous Fe given to fasting subjects in a solution containing 30 mg ascorbic acid and that of Fe in a rice meal (48.7 and 3.5% respectively).5. When ascorbic acid was added during cooking there was a threefold increase in the absorption of both intrinsic Fe and supplementary Fe when a sufficient quantity (60 mg) was present.6. It is concluded that the Fe nutrition of rice-eating communities could be improved significantly by the addition of ascorbic acid to the diet.

Effects of cytochrome P-450 inhibitors on ionic currents in isolated rat type I carotid body cells

1996 ◽  
Vol 271 (1) ◽  
pp. C85-C92 ◽  
Author(s):  
C. J. Hatton ◽  
C. Peers
Keyword(s):  
Carotid Body ◽  
Single Channel ◽  
Ionic Currents ◽  
K Channel ◽  
Type I ◽  
Type I Cells ◽  
Channel Inhibition ◽  
Cytochrome P 450 ◽  
I Cells ◽  
K Currents

Hypoxic chemoreception in the carotid body involves selective inhibition of K+ channels in type I cells. We have investigated whether cytochrome P-450 may act as an O2 sensor coupling hypoxia to K+ channel inhibition, by investigating the actions of P-450 inhibitors to modulate channel activity (recorded using patch-clamp techniques) in type I cells isolated from 8-to 12-day-old rat pups. The imidazole antimycotic P-450 inhibitors miconazole and clotrimazole (1-10 microM) inhibited the Ca(2+)-activated (KCa) and voltage-gated K+ (Kv) currents in isolated type I cells. Single-channel recordings indicated that the KCa channels could be inhibited directly by miconazole. Miconazole also irreversibly inhibited Ca2+ channel currents. By contrast, acute application of the suicide substrate P-450 inhibitor, 1-aminobenzotriazole (1-ABT; 3 mM) was without effect on K+ or Ca2+ currents. Hypoxia (16-23 mmHg) reversibly inhibited K+ currents and prevented the inhibitory actions of miconazole. Furthermore, the inhibitory actions of miconazole could be partially reversed by hypoxia. Pretreatment of cells for 60 min with 3 mM 1-ABT substantially reduced the inhibitory actions of hypoxia on K+ currents. Our results indicate that imidazole antimycotic P-450 inhibitors can directly and nonselectively inhibit ionic channels in type I cells but, more importantly, provide evidence to suggest that hypoxic inhibition of K+ currents in type I cells is mediated in part at least by cytochrome P-450.

Membrane currents recorded from a fragment of rabbit intestinal smooth muscle cell

1986 ◽  
Vol 251 (3) ◽  
pp. C335-C346 ◽  
Author(s):  
Y. Ohya ◽  
K. Terada ◽  
K. Kitamura ◽  
H. Kuriyama
Keyword(s):  
Smooth Muscle ◽  
Longitudinal Muscle ◽  
Outward Current ◽  
Ionic Currents ◽  
Muscle Layer ◽  
Dependent Manner ◽  
Rabbit Ileum ◽  
Longitudinal Muscle Layer ◽  
Inward Current ◽  
K Currents

Properties of ionic currents in smooth muscle membranes of the longitudinal muscle layer of the rabbit ileum were investigated using the single electrode voltage clamp method. In the present experiments, this method was applicable only to the smooth muscle ball (fragment) and not for the dispersed whole cell, because of incompleteness of the voltage clamping. A voltage step elicited a transient inward current followed by an outward current. This outward current was partly inhibited by Mn2+ or nisoldipine or by a reduction in the extracellular [Ca2+] ([Ca2+]o). Tetraethylammonium (TEA) reduced the delayed outward current in a dose-dependent manner, but 50 mM TEA did not produce a complete block of a residual current. When the pipette contained K+-free (Cs+ with TEA+) solution, the residual outward current was abolished. The inward current was elicited at -30 mV (holding potential of -60 mV) and reached the maximal value at +10 mV; the polarity was reversed at +60 mV. This inward current depended on the [Ca2+]o and was blocked by Mn2+ or nisoldipine. Ba2+ also permeated the membrane, and the inward current evoked by Ba2+ was also blocked by Mn2+ or nisoldipine. Reduction of [Na+]o in a solution containing 2.4 mM Ca2+ neither modified the current-voltage relation nor the decay of the inward current, but when [Ca2+]o was reduced to below 1 microM, Na+ permeated the membrane and was blocked by nisoldipine. In conclusion, ionic currents were recordable from the fragmented ball of the longitudinal muscle of rabbit ileum. There were at least two K+ currents as the outward current (Ca2+-dependent K+ and delayed K+ currents) and a Ca2+ current as the inward current. The property of the Ca2+ channel was similar to that observed with other preparations.

scholarly journals Apamin Does Not Inhibit Human Cardiac Na+ Current, L-type Ca2+ Current or Other Major K+ Currents

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e96691 ◽  
Author(s):  
Chih-Chieh Yu ◽  
Tomohiko Ai ◽  
James N. Weiss ◽  
Peng-Sheng Chen
Keyword(s):  
Na Current ◽  
K Currents
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