scholarly journals Calcium currents in bullfrog sympathetic neurons. I. Activation kinetics and pharmacology.

1989 ◽  
Vol 94 (1) ◽  
pp. 151-167 ◽  
Author(s):  
S W Jones ◽  
T N Marks
Keyword(s):  
Calcium Current ◽  
Sympathetic Neurons ◽  
Bay K 8644 ◽  
Calcium Currents ◽  
Type Model ◽  
Muscarinic Agonists ◽  
Activation Kinetics ◽  
Monovalent Ions ◽  
Inward Currents ◽  
A Minor

The calcium current of bullfrog sympathetic neurons activates and deactivates rapidly (tau less than 3 ms). For brief depolarizations, the current can be fit reasonably well by a Hodgkin-Huxley-type model with a single gating particle of charge +3. With 2 mM Ca2+ as the charge carrier, half-maximal activation occurs at approximately -5 mV, near the voltage where activation and deactivation are slowest. When extracellular divalent ion concentrations are reduced, monovalent ions (e.g., Na+ and methylammonium) produce kinetically similar inward currents. Current carried by Ba2+ is blocked by Cd2+ at micromolar concentrations, and by 100 nM omega-conotoxin. Commercially available saxitoxin blocks the current, but different batches have quantitatively different potency. The dihydropyridine agonist Bay K 8644 induces a slight shift in activation kinetics to more negative voltages, with little effect on the peak current. Nifedipine at least partially reverses the effect of Bay K 8644, but has little effect on its own. Muscarinic agonists and other ligands that inhibit the M-type potassium current of frog sympathetic neurons have weak inhibitory effects on the calcium current as well. One interpretation of these results is that the N-type calcium current predominates in these cells, with a minor contribution of L-type current.

Separation and modulation of calcium currents in bullfrog sympathetic neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S56-S63 ◽  
Author(s):  
Stephen W. Jones ◽  
Keith S. Elmslie
Keyword(s):  
G Protein ◽  
Calcium Current ◽  
Sympathetic Neurons ◽  
Calcium Currents ◽  
Dependent Manner ◽  
Activation Kinetics ◽  
Channel Opening ◽  
Voltage Dependent ◽  
Rapid Activation ◽  
Kinetics Of

The calcium current of frog sympathetic neurons has relatively rapid activation kinetics (τ < 3 ms) in response to changes in voltage. Pharmacologically, the current is blocked ~90% by ω-conotoxin, but < 10% by dihydropyridine antagonists. This suggests that nearly all of the current is N type. However, inactivation is slow and incomplete even for depolarizations lasting > 1 s, consistent with recent evidence that N-type channels do not always inactivate rapidly. The calcium current is partially inhibited via receptors for acetylcholine, luteinizing hormone releasing hormone, substance P, ATP, and norepinephrine. These effects are mimicked by internal dialysis with GTP-γ-S, suggesting involvement of a G protein. The transmitters affect the activation kinetics of the calcium current in a voltage-dependent manner, which can be modeled as a reversible shift of some channels to "reluctant" states in which strong depolarization is needed to produce channel opening. The effects of transmitters develop and recover with t½ ~ 1–2 s, so if a second messenger is involved in receptor – calcium channel coupling, it must act rapidly.Key words: norepinephrine, ω-conotoxin, dihydropyridine, inactivation, G protein.

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.

Selective disruption by protein kinases of G-protein-mediated Ca2+ channel modulation

1996 ◽  
Vol 76 (1) ◽  
pp. 311-320 ◽  
Author(s):  
M. S. Shapiro ◽  
J. Zhou ◽  
B. Hille
Keyword(s):  
Protein Kinase ◽  
G Protein ◽  
Kinase Inhibitor ◽  
Sympathetic Neurons ◽  
Calcium Currents ◽  
Muscarinic Agonists ◽  
Whole Cell Patch Clamp ◽  
Cervical Ganglion ◽  
K Current ◽  
M1 Muscarinic

1. We studied the effects of phorbol-12-myristate, 13-acetate (PMA) on G-protein-mediated inhibition of Ca2+ channels by several neurotransmitters in rat superior cervical ganglion (SCG) sympathetic neurons, with the use of the whole cell patch clamp. PMA attenuated membrane-delimited inhibition of calcium currents (ICa) by norepinephrine (NE) and somatostatin by more than half, but did not attenuate inhibition by M1 muscarinic receptors, which use a diffusible cytoplasmic messenger. Inhibition of ICa by NE through pertussis-toxin-sensitive and -insensitive G proteins was equally attenuated by PMA. PMA enhanced ICa in about half the neurons (enhancement of 10 +/- 1%, mean +/- SE) and strongly reduced the holding current in 44 of 61 cells. 2. The M-type K+ current (IM) was not suppressed by PMA, and PMA did not attenuate inhibition of IM by muscarinic agonists, which is also via a diffusible cytoplasmic messenger. 3. Attenuation of NE and somatostatin inhibition by PMA was blocked by 1 microM staurosporine, a broad-spectrum protein kinase inhibitor. Tests with three inhibitors selective for distinct isoforms of protein kinase C (PKC) gave mixed results. PMA's actions were unaffected by 1 microM calphostin C, blocked by 500 nM bisindolylmaleimide, and unaffected by the pseudosubstrate inhibitor PKC19-36. 4. Thus we find that two membrane-delimited signaling pathways that inhibit ion channels in rat SCG neurons are strongly attenuated by PMA, but signaling pathway(s) that use a diffusible cytoplasmic messenger are not. We speculate that a nonstandard PKC isoform, perhaps PKC mu, mediates PMA actions.

Characterization of inward currents and channels underlying burst activity in motoneurons of crab cardiac ganglion

2013 ◽  
Vol 110 (1) ◽  
pp. 42-54 ◽  
Author(s):  
Joseph L. Ransdell ◽  
Simone Temporal ◽  
Nicole L. West ◽  
Megan L. Leyrer ◽  
David J. Schulz
Keyword(s):  
Calcium Channel ◽  
Calcium Current ◽  
Sodium Current ◽  
Large Cell ◽  
Calcium Currents ◽  
Cardiac Ganglion ◽  
Cancer Borealis ◽  
Cationic Current ◽  
Inward Currents

Large cell motoneurons in the Cancer borealis cardiac ganglion generate rhythmic bursts of action potentials responsible for cardiac contractions. While it is well known that these burst potentials are dependent on coordinated interactions among depolarizing and hyperpolarizing conductances, the depolarizing currents present in these cells, and their biophysical characteristics, have not been thoroughly described. In this study we used a combined molecular biology and electrophysiology approach to look at channel identity, expression, localization, and biophysical properties for two distinct high-voltage-activated calcium currents present in these cells: a slow calcium current ( ICaS) and a transient calcium current ( ICaT). Our data indicate that CbCaV1 is a putative voltage-gated calcium channel subunit in part responsible for an L-type current, while CbCaV2 (formerly cacophony) is a subunit in part responsible for a P/Q-type current. These channels appear to be localized primarily to the somata of the motoneurons. A third calcium channel gene (CbCaV3) was identified that encodes a putative T-type calcium channel subunit and is expressed in these cells, but electrophysiological studies failed to detect this current in motoneuron somata. In addition, we identify and characterize for the first time in these cells a calcium-activated nonselective cationic current ( ICAN), as well as a largely noninactivating TTX-sensitive current reminiscent of a persistent sodium current. The identification and further characterization of these currents allow both biological and modeling studies to move forward with more attention to the complexity of interactions among these distinct components underlying generation of bursting output in motoneurons.

Differential neuromodulation of calcium currents by norepinephrine in rat sympathetic neurons

1993 ◽  
Vol 70 (4) ◽  
pp. 1440-1450 ◽  
Author(s):  
C. Chen ◽  
G. G. Schofield
Keyword(s):  
Sympathetic Neurons ◽  
Bay K 8644 ◽  
Current Amplitude ◽  
Calcium Currents ◽  
Response Curves ◽  
Patch Clamp Technique ◽  
Tail Current ◽  
Significant Difference ◽  
Cervical Ganglion ◽  
Cell Capacitance

1. Differences in the neuromodulation of Ca2+ currents between superior cervical ganglion (SCG) and more caudal paravertebral ganglion (PVG) neurons acutely isolated from the same rats were investigated using the whole-cell patch-clamp technique. 2. Norepinephrine (NE) induced a concentration-dependent inhibition of Ca2+ currents in both SCG and PVG neurons. The concentration producing 50% inhibition (IC50) for NE estimated from concentration-response curves was similar between SCG and PVG neurons but the maximal inhibition estimated from the concentration-response curve for PVG neurons was decreased compared with that of SCG neurons. 3. Tail current activation curves of both SCG and PVG neurons in the absence and presence of NE (5 microM) could be fitted to a double Boltzmann equation. In the presence of NE, the activation curves for both SCG and PVG neurons were shifted toward more depolarized potentials. The magnitude of the shift was greater in SCG than in PVG neurons, which could be accounted for by a greater decrease (P < 0.05) in the fractional amplitude of the first current component of SCG neurons (delta 1.4 +/- 0.4 nA, mean +/- SE, 39%) compared with that of PVG neurons (delta 0.9 +/- 0.1 nA, 16%). 4. Ca2+ current density, expressed as maximal tail current amplitude normalized to cell capacitance, was greater in PVG neurons than that in SCG neurons. 5. In SCG neurons, a saturating concentration of omega-conotoxin GVIA (omega-CgTx) produced a greater decrease of Ca2+ current amplitude at +20 mV (77.4 +/- 1.9%) than in PVG neurons (71.2 +/- 1.5%, P < 0.05). 6. After pretreatment with 15 microM omega-CgTx, NE still decreased the Ca2+ currents in both populations of neurons; however, the inhibition was greater in SCG neurons (31.1 +/- 3.4%) than in PVG neurons (12.8 +/- 3.6%, P < 0.01). 7. The dihydropyridine Ca2+ channel "agonist" Bay K 8644 (10 microM) prolonged Ca2+ tail currents in both SCG and PVG neurons. After normalizing to cell capacitance, there was no significant difference in Bay K 8644-induced tail current amplitude between the two populations of neurons. Moreover, NE (5 microM) increased the prolonged Ca2+ tail current amplitude induced by Bay K 8644 (10 microM) by 44.7 +/- 13.5% in SCG and 41.9 +/- 11.9% in PVG neurons. 8. Under control conditions, Ca2+ currents were facilitated by a depolarizing conditioning pulse (50 ms to +100 mV) in both PVG neurons (29.2 +/- 5.1%) and SCG neurons (20.1 +/- 4.0%).(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium currents in turtle retinal ganglion cells. I. The properties of T- and L-type currents

1994 ◽  
Vol 71 (2) ◽  
pp. 733-742 ◽  
Author(s):  
Y. Liu ◽  
E. M. Lasater
Keyword(s):  
Retinal Ganglion Cells ◽  
Calcium Current ◽  
Ganglion Cells ◽  
Bay K 8644 ◽  
Calcium Currents ◽  
Retinal Ganglion ◽  
Transient Component ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Sodium And Potassium

1. Voltage-activated calcium currents from single, isolated turtle retinal ganglion cells were characterized with standard whole cell patch clamp techniques. Calcium current amplitude was increased with the use of 10 mM extracellular Ca2+, whereas sodium and potassium currents were pharmacologically suppressed. 2. A transient component, expressed in approximately 39% of the cells recorded from, closely resembled the T-type calcium current described previously in other tissues. This component activated at low voltages (around -50 mV from a holding potential of -70 mV) and inactivated with a time constant 10-30 ms at -20 mV; the inactivation was strongly voltage dependent. Substitution of Ca2+ with Ba2+ reduced this current in most cases or had no effect in some instances. Surprisingly, the transient calcium current was potentiated by Bay-K 8644 and inhibited by nifedipine in some of the ganglion cells tested. 3. A sustained component, which activated at between -20 and -10 mV from a holding potential of -70 mV, was found in all ganglion cells from which we recorded. This component was substantially larger when equimolar Ba2+ replaced Ca2+ as the charge carrier, and was sensitive to the dihydropyridine agonist Bay-K 8644 and the antagonist nifedipine. Thus the sustained current in turtle retinal ganglion cells was similar to the L-type calcium current described in chick DRG neurons. However, unlike the typical L-type current, this component in turtle ganglion cells showed an inactivation that was highly dependent on the intracellular free Ca2+ concentration but not the membrane potential. 4. Synthetic omega-conotoxin MVIIC selectively blocked the sustained calcium current while sparing the transient component. It could completely block the sustained current that was resistant to nifedipine in some cells. Thus there may exist several different high voltage-activated calcium channels in turtle retinal ganglion cells.

Calcium currents from jellyfish striated muscle cells: preservation of phenotype, characterisation of currents and channel localisation

2001 ◽  
Vol 204 (21) ◽  
pp. 3717-3726
Author(s):  
Y.-C. James Lin ◽  
Andrew N. Spencer
Keyword(s):  
Calcium Current ◽  
Striated Muscle ◽  
Ionic Current ◽  
Muscle Cells ◽  
Ionic Currents ◽  
Calcium Currents ◽  
Nickel Ions ◽  
Polyorchis Penicillatus ◽  
Inward Currents

SUMMARY When striated muscle cells of the jellyfish Polyorchis penicillatus were dissociated at 30°C they retained their in vivo morphology and the integrity of ionic currents. This contrasted with cells dissociated at room temperature that rarely expressed any inward currents. Whole-cell, patch-clamp recordings from dissociated muscle cells revealed that the inward component of the total ionic current consisted of only one calcium current. This calcium current activated at –70 mV, peaked at –30 mV, and inactivated within 5 ms. In comparison with barium and strontium ions, calcium ions were the preferred current carriers. Calcium channels can be blocked by dihydropyridines and nickel ions at micromolar levels. Several properties of this current are reminiscent of T-type calcium currents. Localisation of this channel using the fluorescent channel blocker fDHP and the fluorescent dye RH414 indicated that myofibres had a higher density of these channels than the somata.

R-type calcium channels in myenteric neurons of guinea pig small intestine

2004 ◽  
Vol 287 (1) ◽  
pp. G134-G142 ◽  
Author(s):  
Xiaochun Bian ◽  
Xiaoping Zhou ◽  
James J. Galligan
Keyword(s):  
Guinea Pig ◽  
Calcium Channels ◽  
Calcium Current ◽  
Calcium Currents ◽  
Voltage Sensitivity ◽  
Total Calcium ◽  
Myenteric Neurons ◽  
Combined Application ◽  
Inward Currents ◽  
Rapid Activation

Currents carried by L-, N-, and P/Q-type calcium channels do not account for the total calcium current in myenteric neurons. This study identified all calcium channels expressed by guinea pig small intestinal myenteric neurons maintained in primary culture. Calcium currents were recorded using whole cell techniques. Depolarizations (holding potential = −70 mV) elicited inward currents that were blocked by CdCl2 (100 μM). Combined application of nifedipine (blocks L-type channels), Ω-conotoxin GVIA (blocks N-type channels), and Ω-agatoxin IVA (blocks P/Q-type channels) inhibited calcium currents by 56%. Subsequent addition of the R-type calcium channel antagonists, NiCl2 (50 μM) or SNX-482 (0.1 μM), abolished the residual calcium current. NiCl2 or SNX-482 alone inhibited calcium currents by 46%. The activation threshold for R-type calcium currents was −30 mV, the half-activation voltage was −5.2 ± 5 mV, and the voltage sensitivity was 17 ± 3 mV. R-type currents activated fully in 10 ms at 10 mV. R-type calcium currents inactivated in 1 s at 10 mV, and they inactivated (voltage sensitivity of 16 ± 1 mV) with a half-inactivation voltage of −76 ± 5 mV. These studies have accounted for all of the calcium channels in myenteric neurons. The data indicate that R-type calcium channels make the largest contribution to the total calcium current in myenteric neurons. The relatively positive half-activation voltage and rapid activation kinetics suggest that R-type channels could contribute to calcium entry during somal action potentials or during action potential-induced neurotransmitter release.

Control of calcium current in rat sympathetic neurons by norepinephrine

1982 ◽  
Vol 244 (1) ◽  
pp. 135-144 ◽  
Author(s):  
Martin Galvan ◽  
Paul R. Adams
Keyword(s):  
Calcium Current ◽  
Sympathetic Neurons
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