Selective Potentiation of L-Type Calcium Channel Currents by Cocaine in Cardiac Myocytes

1999 ◽  
Vol 56 (6) ◽  
pp. 1138-1142 ◽  
Author(s):  
Louis S. Premkumar
Keyword(s):  
Calcium Channel ◽  
Cardiac Myocytes ◽  
Channel Currents

Decreased calcium channel currents and facilitated epinephrine release in the Ca2+ channel β3 subunit-null mice

2010 ◽  
Vol 394 (3) ◽  
pp. 464-469 ◽  
Author(s):  
Toshio Ohta ◽  
Takayoshi Ohba ◽  
Takashi Suzuki ◽  
Hiroyuki Watanabe ◽  
Hironobu Sasano ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Channel Currents

CALCIUM CHANNEL CURRENTS IN NEURONES FROM LOCUST (SCHISTOCERCA GREGARIA) THORACIC GANGLIA

1993 ◽  
Vol 177 (1) ◽  
pp. 201-221 ◽  
Author(s):  
H. A. Pearson ◽  
G. Lees ◽  
D. Wray
Keyword(s):  
Calcium Channel ◽  
Single Channel ◽  
Schistocerca Gregaria ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Transient Component ◽  
Thoracic Ganglia ◽  
Steady State Inactivation ◽  
Inward Currents ◽  
Channel Currents

1. Using the patch-clamp technique, Ca2+ channel currents were recorded from neurones freshly isolated from the thoracic ganglia of the desert locust Schistocerca gregaria. 2. In solutions containing 10 mmol l-1 Ba2+ we observed high-voltage-activated whole-cell inward currents with sustained and transient components, both of which had similar steady-state inactivation properties. 3. Substitution of Ca2+ for Ba2+ was found to reduce whole-cell currents, whereas removal of monovalent cations had no effect. 4. Cd2+ (1 mmol l-1) completely blocked the whole-cell current, but at 10 micromolar preferentially inhibited the sustained component without affecting the transient component. 5. Verapamil (1 micromolar) inhibited both current components but appeared to be more selective for the sustained component, whereas nitrendipine (1 micromolar) had no effect on either component. 6. A single-channel recording suggested that the transient component was carried by a low- conductance channel. 7. Certain compounds with insecticidal action (ryanodine, S-bioallethrin, deltamethrin and avermectin) did not affect calcium channel currents in these cells. 8. These data suggest that there are two types of Ca2+ channels present in locust neurones. These channel types have properties differing from the T-, L- and N-type channels found in vertebrates and, furthermore, were not targets for the insecticides we tested.

scholarly journals M4 Muscarinic Receptor Activation Modulates Calcium Channel Currents in Rat Intracardiac Neurons

1997 ◽  
Vol 78 (4) ◽  
pp. 1903-1912 ◽  
Author(s):  
J. Cuevas ◽  
D. J. Adams
Keyword(s):  
Calcium Channel ◽  
Muscarinic Receptor ◽  
High Voltage ◽  
Receptor Activation ◽  
Muscarinic Agonist ◽  
Muscarinic Agonists ◽  
Maximal Inhibition ◽  
Cell Recording ◽  
Channel Currents ◽  
Intracardiac Neurons

Cuevas, J. and Adams, D. J. M4 muscarinic receptor activation modulates calcium channel currents in rat intracardiac neurons. J. Neurophysiol. 78: 1903–1912, 1997. Modulation of high-voltage–activated Ca2+ channels by muscarinic receptor agonists was investigated in isolated parasympathetic neurons of neonatal rat intracardiac ganglia using the amphotericin B perforated-patch whole cell recording configuration of the patch-clamp technique. Focal application of the muscarinic agonists acetylcholine (ACh), muscarine, and oxotremorine-M to the voltage-clamped soma membrane reversibly depressed peak Ca2+ channel current amplitude. The dose-reponse relationship obtained for ACh-induced inhibition of Ba2+ current ( I Ba) exhibited a half-maximal inhibition at 6 nM. Maximal inhibition of I Ba amplitude obtained with 100 μM ACh was ∼75% compared with control at +10 mV. Muscarinic agonist-induced attenuation of Ca2+ channel currents was inhibited by the muscarinic receptor antagonists pirenzepine (≤300 nM) and m4-toxin (≤100 nM), but not by AF-DX 116 (300 nM) or m1-toxin (60 nM). The dose-response relationship obtained for antagonism of muscarine-induced inhibition of I Ba by m4-toxin gave an IC50 of 11 nM. These results suggest that muscarinic agonist-induced inhibition of high-voltage–activated Ca2+ channels in rat intracardiac neurons is mediated by the M4 muscarinic receptor. M4 receptor activation shifted the voltage dependence and depressed maximal activation of Ca2+ channels but had no effect on the steady-state inactivation of Ca2+ channels. Peak Ca2+ channel tail current amplitude was reduced ≥30% at +90 mV in the presence of ACh, indicating a voltage-independent component to the muscarinicreceptor-mediated inhibition. Both dihydropyridine- and ω-conotoxin GVIA–sensitive and -insensitive Ca2+ channels were inhibited by ACh, suggesting that the M4 muscarinic receptor is coupled to multiple Ca2+ channel subtypes in these neurons. Inhibition of I Ba amplitude by muscarinic agonists was also observed after cell dialysis using the conventional whole cell recording configuration. However, internal perfusion of the cell with 100 μM guanosine 5′-O-(2-thiodiphosphate) trilithium salt (GDP-β-S) or incubation of the neurons in Pertussis toxin (PTX) abolished the modulation of I Ba by muscarinic receptor agonists, suggesting the involvement of a PTX-sensitive G-protein in the signal transduction pathway. Given that ACh is the principal neurotransmitter mediating vagal innervation of the heart, the presence of this inhibitory mechanism in postganglionic intracardiac neurons suggests that it may serve for negative feedback regulation.

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