scholarly journals Ionic currents in two strains of rat anterior pituitary tumor cells.

1984 ◽  
Vol 83 (3) ◽  
pp. 309-339 ◽  
Author(s):  
J M Dubinsky ◽  
G S Oxford
Keyword(s):  
Rate Constant ◽  
Pituitary Tumor ◽  
Calcium Current ◽  
Potassium Current ◽  
Sodium Current ◽  
Outward Current ◽  
Potassium Currents ◽  
Ionic Currents ◽  
Calcium Currents ◽  
Voltage Dependent

The ionic conductance mechanisms underlying action potential behavior in GH3 and GH4/C1 rat pituitary tumor cell lines were identified and characterized using a patch electrode voltage-clamp technique. Voltage-dependent sodium, calcium, and potassium currents and calcium-activated potassium currents were present in the GH3 cells. GH4/C1 cells possess much less sodium current, less voltage-dependent potassium current, and comparable amounts of calcium current. Voltage-dependent inward sodium current activated and inactivated rapidly and was blocked by tetrodotoxin. A slower-activating voltage-dependent inward calcium current was blocked by cobalt, manganese, nickel, zinc, or cadmium. Barium was substituted for calcium as the inward current carrier. Calcium tail currents decay with two exponential components. The rate constant for the slower component is voltage dependent, while the faster rate constant is independent of voltage. An analysis of tail current envelopes under conditions of controlled ionic gradients suggests that much of the apparent decline of calcium currents arises from an opposing outward current of low cationic selectivity. Voltage-dependent outward potassium current activated rapidly and inactivated slowly. A second outward current, the calcium-activated potassium current, activated slowly and did not appear to reach steady state with 185-ms voltage pulses. This slowly activating outward current is sensitive to external cobalt and cadmium and to the internal concentration of calcium. Tetraethylammonium and 4-aminopyridine block the majority of these outward currents. Our studies reveal a variety of macroscopic ionic currents that could play a role in the initiation and short-term maintenance of hormone secretion, but suggest that sodium channels probably do not make a major contribution.

Potassium currents of neurons isolated from medical nucleus tractus solitarius

1993 ◽  
Vol 265 (5) ◽  
pp. H1596-H1602 ◽  
Author(s):  
J. P. Moak ◽  
D. L. Kunze
Keyword(s):  
Potassium Current ◽  
Voltage Dependence ◽  
Nucleus Tractus Solitarius ◽  
Outward Current ◽  
Potassium Currents ◽  
Afferent Input ◽  
Calcium Currents ◽  
Voltage Dependent ◽  
Current Relaxation ◽  
Outward Potassium Current

Voltage-dependent potassium currents of neurons enzymatically isolated from the medial and dorsal subnuclei of the solitary tract (mNTS) of adult guinea pig have been characterized with respect to their voltage dependence, time dependence, and sensitivity to specific blocking agents. This region of the medulla receives baroreceptor afferent input and is involved in cardiovascular regulation. Our results showed the presence of three types of potassium currents. First, in all neurons studied (n = 58) a slowly developing outward current was present at potentials more positive than -30 mV. The time to half-peak current decreased with depolarization [24.8 ms at 0 mV; 19.2 ms at +10 mV; 12.5 ms at +20 mV; 9.9 ms at +30 mV (n = 4)]. This current required 20 mM tetraethylammonium (TEA) for full block and failed to show significant inactivation for voltage commands up to 300 ms. Second, a rapidly activating, 4-aminopyridine (4-AP)-sensitive transient outward potassium current was present in 83% of the cells examined (n = 39/47). Threshold for activation was -30 mV. The current relaxation consisted of three components: tau 1 = 14-49 ms; tau 2 = 174-362; tau 3 = 1.1-2.4 s. Finally, in all cells tested calcium activated a large nontransient outward potassium current that was inhibited by charybdotoxin. The studies reported here will be used in conjunction with studies describing sodium and calcium currents to understand the basis for generation of activity in the mNTS in response to baroreceptor input.

A background sodium conductance is necessary for spontaneous depolarizations in rat pituitary cell line GH3

1994 ◽  
Vol 266 (3) ◽  
pp. C709-C719 ◽  
Author(s):  
S. M. Simasko
Keyword(s):  
Cell Line ◽  
Calcium Current ◽  
Membrane Conductance ◽  
Potassium Currents ◽  
Pituitary Cell ◽  
Calcium Currents ◽  
Gh3 Cells ◽  
Sodium Conductance ◽  
Rat Pituitary ◽  
Voltage Dependent

The role of Na+ in the expression of membrane potential activity in the clonal rat pituitary cell line GH3 was investigated using the perforated patch variation of patch-clamp electrophysiological techniques. It was found that replacing bath Na+ with choline, tris(hydroxymethyl)aminomethane (Tris), or N-methyl-D-glucamine (NMG) caused the cells to hyperpolarize 20-30 mV. Tetrodotoxin had no effect. The effects of the Na+ substitutes could not be explained by effects on potassium or calcium currents. Although all three Na+ substitutes suppressed voltage-dependent calcium current by 10-20%, block of voltage-dependent calcium current by nifedipine or Co2+ did not result in hyperpolarization of the cells. There was no effect of the Na+ substitutes on voltage-dependent potassium currents. In contrast, all three Na+ substitutes influenced calcium-activated potassium currents [IK(Ca)], but only at depolarized potentials. Choline consistently suppressed IK(Ca), whereas Tris and NMG either had no effect or slightly increased IK(Ca). These effects on IK(Ca) also cannot explain the hyperpolarization induced by removing bath Na+. Choline always hyperpolarized cells yet suppressed IK(Ca). Furthermore, removing bath Na+ caused an increase in cell input resistance, an observation consistent with the loss of a membrane conductance as the basis of the hyperpolarization. Direct measurement of background currents revealed a 12-pA inward current at -84 mV that was lost upon removing bath Na+. These results suggest that this background sodium conductance provides the depolarizing drive for GH3 cells to reach the threshold for firing calcium-dependent action potentials.

scholarly journals Effect of FMRFamide on voltage-dependent currents in identified centrifugal neurons of the optic lobe of the cuttlefish, Sepia officinalis

2020 ◽  
Author(s):  
Abdesslam Chrachri
Keyword(s):  
Visual Processing ◽  
Calcium Current ◽  
Optic Lobe ◽  
Low Voltage ◽  
Sodium Current ◽  
Calcium Currents ◽  
Delayed Rectifier ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents

AbstractWhole-cell patch-clamp recordings from identified centrifugal neurons of the optic lobe in a slice preparation allowed the characterization of five voltage-dependent currents; two outward and three inward currents. The outward currents were; the 4-aminopyridine-sensitive transient potassium or A-current (IA), the TEA-sensitive sustained current or delayed rectifier (IK). The inward currents were; the tetrodotoxin-sensitive transient current or sodium current (INa). The second is the cobalt- and cadmium-sensitive sustained current which is enhanced by barium and blocked by the dihydropyridine antagonist, nifedipine suggesting that it could be the L-type calcium current (ICaL). Finally, another transient inward current, also carried by calcium, but unlike the L-type, this current is activated at more negative potentials and resembles the low-voltage-activated or T-type calcium current (ICaT) of other preparations.Application of the neuropeptide FMRFamide caused a significant attenuation to the peak amplitude of both sodium and sustained calcium currents without any apparent effect on the transient calcium current. Furthermore, FMRFamide also caused a reduction of both outward currents in these centrifugal neurons. The fact that FMRFamide reduced the magnitude of four of five characterized currents could suggest that this neuropeptide may act as a strong inhibitory agent on these neurons.SummaryFMRFamide modulate the ionic currents in identified centrifugal neurons in the optic lobe of cuttlefish: thus, FMRFamide could play a key role in visual processing of these animals.

Voltage-dependent ionic currents in solitary horizontal cells isolated from cat retina

1992 ◽  
Vol 68 (4) ◽  
pp. 1143-1150 ◽  
Author(s):  
Y. Ueda ◽  
A. Kaneko ◽  
M. Kaneda
Keyword(s):  
Potassium Current ◽  
Horizontal Cell ◽  
Potassium Currents ◽  
Ionic Currents ◽  
Horizontal Cells ◽  
Membrane Properties ◽  
Resting Potential ◽  
Delayed Rectifier ◽  
Cat Retina ◽  
Voltage Dependent

1. Horizontal cells of the cat retina were isolated by enzymatic dissociation. Two types of horizontal cells were identified: the axonless (A-type) horizontal cell having four to six thick, long (approximately 100 microns) dendrites, and the short-axon (B-type) horizontal cell having many (> 5) fine, short (approximately 30 microns) dendrites. 2. Membrane properties of isolated horizontal cells were analyzed under current-clamp and voltage-clamp conditions. In the A-type cell, the average resting potential was -55 mV and the mean membrane capacitance was 110 pF, whereas values in the B-type cell were -58 mV and 40 pF, respectively. The A-type cell showed long-lasting Ca spikes, but B-type cells had no Ca spikes. 3. Five types of voltage-dependent ionic currents were recorded: a sodium current (INa), a calcium current (ICa), and three types of potassium currents. Potassium currents consisted of potassium current through the inward rectifier (Ianomal), transient outward potassium current (IA), and potassium current through the delayed rectifier (IK(v)). INa was recorded only from A-type cells. Other currents were recorded from both types of cells. 4. INa activated when cells were depolarized from a holding potential (Vh) of -95 mV, and it was maximal at -25 mV. This current was blocked by tetrodotoxin. Approximately half of the A-type cells had INa, but no B-type cell had this current. 5. L-type ICa, an inward-going sustained current, was activated with depolarization more positive than -25 mV. Current amplitude reached a maximal value near 15 mV and became smaller with further depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Potassium currents contributing to action potential repolarization and the afterhyperpolarization in rat vagal motoneurons

1992 ◽  
Vol 68 (5) ◽  
pp. 1834-1841 ◽  
Author(s):  
P. Sah ◽  
E. M. McLachlan
Keyword(s):  
Action Potential ◽  
Time Constant ◽  
Action Potentials ◽  
Potassium Current ◽  
Outward Current ◽  
Potassium Currents ◽  
Membrane Potentials ◽  
Calcium Currents ◽  
Resting Potential ◽  
Action Potential Repolarization

1. Intracellular recordings were made from neurons in the dorsal motor nucleus of the vagus (DMV) in transverse slices of rat medulla maintained in vitro at 30 degrees C. Neurons had a resting potential of -59.8 +/- 1.4 (SE) mV (n = 39) and input resistance of 293 +/- 23 M omega (n = 44). 2. Depolarization elicited overshooting action potentials that were blocked by tetrodotoxin (TTX; 1 microM). In the presence of TTX, two types of action potentials having low and high thresholds could be elicited. The action potentials were blocked by cobalt (2 mM) indicating they were mediated by calcium currents. 3. Under voltage clamp, depolarization of the cell from membrane potentials negative of the resting potential activated a transient potassium current. This current was selectively blocked by 4-aminopyridine (4-AP) (5 mM) and catechol (5 mM) indicating that it is an A-type current. This current inactivated with a time constant of 420 ms and recovered from inactivation with a time constant of 26 ms. 4. When calcium currents were blocked by cadmium or cobalt, the rate of action potential repolarization was slower. In the presence of tetraethylammonium (TEA; 200-400 microM) or charybdotoxin (CTX; 30 nM) a small "hump" appeared on the repolarizing phase of the action potential that was abolished by addition of cadmium. These results indicate that a calcium-activated potassium current (IC) contributes to action potential repolarization. 5. Actions potentials elicited from hyperpolarized membrane potentials repolarized faster than those elicited from resting membrane potential. This effect could be blocked by catechol, indicating that voltage-dependent potassium currents (IA) can also contribute to action-potential repolarization. In the presence of catechol and calcium channel blockers, action potentials still had a significant early afterhyperpolarization suggesting that another calcium independent outward current is also active during repolarization. This fast afterhyperpolarizations (AHP) was not blocked by TEA. 6. Action potentials were followed by prolonged AHPs, which had two phases. The initial part of the AHP was blocked by apamin (100 nM) indicating that it results from activation of SK type calcium-activated potassium channels. The slow phase was selectively blocked by catechol suggesting that it is due to activation of IA. 7. It is concluded that a TTX-sensitive sodium current and two calcium currents contribute to the action potential in rat DMV neurons. At least three different currents contribute to action-potential repolarization: IC, IA, and a third unidentified calcium-insensitive outward current.(ABSTRACT TRUNCATED AT 400 WORDS)

Voltage-dependent calcium currents in rat gonadotropes separated by centrifugal elutriation

1990 ◽  
Vol 258 (4) ◽  
pp. E589-E596 ◽  
Author(s):  
C. Marchetti ◽  
G. V. Childs ◽  
A. M. Brown
Keyword(s):  
Time Constant ◽  
Calcium Current ◽  
Low Voltage ◽  
Sodium Current ◽  
Ionic Currents ◽  
Physiological Solution ◽  
Calcium Currents ◽  
Pituitary Cells ◽  
Centrifugal Elutriation ◽  
Rat Pituitary Cells

Centrifugal elutriation of rat pituitary cells yielded two functionally active fractions (6 and 7) that contained 30-40 and 50-60% gonadotropes, respectively. We studied the membrane ionic currents of these cells with the whole cell patch-clamp method. In physiological solution, cells from the enriched fractions displayed a tetrodotoxin-sensitive sodium current. In 20 mM external calcium and zero sodium, the inward current contained two components that were different in threshold, steady-state inactivation, and deactivation. One component was half activated at approximately -25 mV, half inactivated from a holding potential of -61 mV, and deactivated with a time constant of 3 ms. The second component was half activated at 6 mV and deactivated with a time constant of 0.35 ms. These two currents resembled the high-voltage-activated and low-voltage-activated calcium current described in many preparations, including clonal and primary pituitary cells. Bath application of 20 nM gonadotropin-releasing hormone caused a transient and reversible decrease of the calcium current at depolarized voltages and a negative shift of 10 mV in the activation curve. Both effects were observed in a percentage of cells that closely matches the percentage of gonadotropes in the fraction. The shift appeared to affect both components of the current and can partially account for the increased activity of Ca2+ channels at potentials close to the resting value.

Nitric Oxide and Histamine Induce Neuronal Excitability by Blocking Background Currents in Neuron MCC of Aplysia

2004 ◽  
Vol 91 (2) ◽  
pp. 656-665 ◽  
Author(s):  
Jon W. Jacklet ◽  
David G. Tieman
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Potassium Current ◽  
Neural Circuit ◽  
Outward Current ◽  
Potassium Currents ◽  
Ionic Currents ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Calcium Dependent

Nitric oxide (NO) and histamine are important neurotransmitters and neuromodulators. We investigated their ability to modulate the membrane ionic currents and excitability of the metacerebral cell (MCC) of Aplysia using voltage clamp techniques. MCC is a serotonergic modulator of the feeding neural circuit. It receives powerful long-lasting excitatory synaptic input mediated by NO and histamine. NO donors reduced a background outward current at and above the resting potential, associated with decreased membrane conductance. This produced a substantial steady-state inward current that was relatively insensitive to cesium or cobalt. The NO response appears to be due to the reduction of a background potassium current and a small increase in persistent inward sodium current. Treatment with 8-bromoguanosine-3′5′-cyclic monophosphate mimics this response, suggesting it is mediated primarily by the NO–guanylyl cyclase–cGMP pathway. In some MCCs, NO blocked an additional potassium current that resulted in current reversal near the potassium equilibrium potential in current–voltage plots. Histamine also reduced a background outward current at and above the resting potential. However, treatment with cobalt, which blocks calcium and calcium-dependent currents, blocked the histamine response, suggesting that histamine decreases calcium activated potassium currents. Although nifedipine (L-type calcium channel blocker) and tetraethylammonium reduced some calcium and calcium-dependent potassium currents, they had only a slight effect on the NO and histamine responses. Both NO and histamine decreased steady-state membrane currents, and thereby depolarized MCC and increased its excitability, but different ionic currents and second messenger pathways are involved, allowing complex state and time dependent modulation of MCC's activity.

The actions of halogenated ethers on the ionic currents of the squid giant axon

1987 ◽  
Vol 231 (1262) ◽  
pp. 13-26 ◽  
Keyword(s):  
Potassium Current ◽  
Time Course ◽  
Sodium Current ◽  
Potassium Currents ◽  
Ionic Currents ◽  
Giant Axon ◽  
Open Circuit ◽  
Course Of Action ◽  
Electrophysiological Effects ◽  
Sodium And Potassium

The effects of fourteen halogenated ethers on the sodium and potassium currents of voltage-clamped squid giant axons have been examined. Effects under open-circuit were also studied. In voltage-clamped axons, the ethers tended to reduce potassium currents at least as much, if not more, than sodium currents. This finding distinguishes the halogenated ethers from many other general anaesthetics. Certain, but not all, halogenated ethers induced a pronounced maximum in potassium current traces as a function of time. This property can be formally described if an inactivation term is added to the Hodgkin– Huxley equation for potassium currents. Large shifts in the sodium-current inactivation parameter h ∞ were produced in some instances. Two fully halogenated methyl ethyl ethers, known to produce convulsions in mice, depressed both sodium and potassium currents, but with a very slow time course of action. The electrophysiological effects of the halogenated ethers investigated appear to depend on the position and number of hydrogen bonds that can be formed.

scholarly journals Modulation of ionic currents by dopamine in an interneurone of the respiratory central pattern generator of Lymnaea stagnalis.

1994 ◽  
Vol 189 (1) ◽  
pp. 37-54 ◽  
Author(s):  
S Barnes ◽  
N I Syed ◽  
A G Bulloch ◽  
K Lukowiak
Keyword(s):  
Calcium Current ◽  
Potassium Current ◽  
Lymnaea Stagnalis ◽  
Outward Current ◽  
Input Resistance ◽  
Ionic Currents ◽  
Pattern Generator ◽  
Spike Threshold ◽  
Inhibitory Mechanisms

Dopamine elicits alternating bursts of activity in the respiratory interneurones of the snail Lymnaea stagnalis. One of the neurones (VD4) was isolated in culture, and the effects of dopamine on both membrane voltage and current were studied utilising the whole-cell tight-seal recording technique. Dopamine had little effect on resting potentials near -60 mV, nor did it affect spike threshold or input resistance measured near -60 mV. However, it did alter the excitability of the cell, changing the response to current injection from one of repetitive spiking to one of rapid accommodation. Under voltage-clamp, VD4 responded to dopamine (EC50 = 92 nmol l-1) with increased net outward current at all potentials more positive than -60 mV. This was due primarily to an increase in voltage-gated potassium current and a decrease in calcium current. A reduction of Cd(2+)-sensitive outward current, possibly calcium-gated potassium current, was also evident at potentials more positive than +60 mV. The physiological actions of dopamine on these cells in vivo are consistent with the inhibitory mechanisms presented in this study.

Guanine nucleotides modulate calcium currents in a marine Paramecium

1993 ◽  
Vol 176 (1) ◽  
pp. 117-133
Author(s):  
J. Bernal ◽  
B. E. Ehrlich
Keyword(s):  
Calcium Channel ◽  
Calcium Current ◽  
Potassium Currents ◽  
Extracellular Calcium ◽  
Guanine Nucleotides ◽  
Calcium Currents ◽  
Freshwater Species ◽  
Cell Functions ◽  
Voltage Dependent ◽  
Gamma S

Voltage-dependent calcium channels play a critical role in many cell functions and in many cell types ranging from protozoa to vertebrates. We have shown previously that guanine nucleotides modulate the calcium action potential and the duration of backward swimming in Paramecium, both indirect measurements of calcium channel function. To determine whether guanine nucleotides to indeed alter calcium currents, the inward calcium current (ICa) in Paramecium calkinsi was studied. First, the calcium current was characterized. The magnitude of ICa increased as the extracellular calcium concentration was increased from 0.5 to 50 mmol l-1, unlike the situation in freshwater species of Paramecium where the inward calcium current magnitude is maximal when extracellular calcium levels reach 1 mmol l-1. Inorganic compounds (NiCl2 at 10 mumol l-1 and CdCl2 at 1 mmol l-1) and organic compounds (naphthalene sulfonamides, W-7 and W-12-Br at 100 and 2 mumol l-1, respectively) reduced ICa. Regardless of the holding membrane potential (from −80 to −20 mV), the threshold activation for ICa was at −10 mV and the maximum value of ICa was reached at +20 mV, suggesting that there is only one type of calcium channel in P. calkinsi. Second, we injected GTP gamma S, GTP and GDP beta S into voltage-clamped cells while monitoring calcium and/or potassium currents. GTP gamma S increased the magnitude of ICa by 42 +/− 6% (mean +/− S.D., N = 5) and the effect was irreversible, GTP increased the magnitude of ICa by 37 +/− 4% (N = 4) in a reversible manner, and GDP beta S decreased ICa by 57 +/− 8% (N = 3) irreversibly. The outward potassium currents did not change when GTP gamma S was injected into the cells. These results support the hypothesis that injection of guanine nucleotides modulates the voltage-dependent calcium channel in P. calkinsi, presumably by activating G-protein-dependent processes.

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