Potassium currents in adult rat intracardiac neurones.

Xi-Moy, S X; Dun, Nae J.

doi:10.1113/jphysiol.1995.sp020787

Cited by 45 publications

(25 citation statements)

References 42 publications

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“…Bath application of 100 M DTG depressed peak voltage-activated K ϩ current amplitude at potentials positive to ϩ20 mV. The voltage dependence and kinetics of the currents observed are consistent with the delayed outwardly rectifying K ϩ current [I K(DR) ] previously reported in intracardiac neurons (Xi-Moy and Dun, 1995). Figure 1B shows a plot of the mean peak I K(DR) amplitude in the absence and presence of DTG as a function of voltage.…”

Section: Methodssupporting

confidence: 59%

“…Haloperidol, ibogaine hydrochloride, (ϩ)-pentazocine, DTG, (ϩ)-SKF-10,047, TTX; tetraethylammonium chloride (TEA), and linopirdine were purchased from Sigma-Aldrich (St. Louis, MO). Xi-Moy and Dun, 1995;Hogg et al, 1999) and express various subunits that contribute to these channels, including KCNA5 and KCNA6 (J. Cuevas, unpublished observation). Given that -1 receptors have been shown to depress heterologously expressed KCNA5 channels (Aydar et al, 2002) and that inhibition of these channels may have significant effects on the function of intracardiac neurons, it seemed prudent to test the effects of receptor activation on currents mediated by voltage-activated K ϩ channels in these cells.…”

Section: Methodsmentioning

confidence: 99%

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σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

Zhang¹,

Cuevas²

2005

J Pharmacol Exp Ther

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The receptors have been implicated in the regulation of the cardiovascular system, and -1 receptor transcripts have been found in parasympathetic intracardiac neurons. However, the cellular function of -1 receptors in these cells remains to be determined. Effects of receptor activation on voltage-activated K ϩ channels and action potential firing were studied in isolated intracardiac neurons using whole-cell patch-clamp recording techniques. Activation of receptors reversibly blocked delayed outwardly rectifying potassium channels, large conductance Ca 2ϩ -sensitive K ϩ channels, and the Mcurrent with maximal inhibition Ͼ80%. The inhibition of K ϩ channels by ligands was dose-dependent, and the rank order potency of (ϩ)-pentazocine Ͼ ibogaine Ͼ 1,3-di-O-tolyguanidin (DTG) suggests that the effect is mediated by -1 receptor activation. Preincubation of neurons with the irreversible receptor antagonist metaphit blocked DTG-induced inhibition of K ϩ channels, confirming that the effect is mediated by receptor activation. Although bath application of ligands depolarized intracardiac neurons, the number of action potentials fired by the cells in response to depolarizing current pulses was decreased in the presence of these drugs. Neither dialysis of the neurons nor application of intracellular 5Ј-O-(2-thiodiphosphate) trilithium salt inhibited the effect of receptors on K ϩ channels, which suggests that the signal transduction pathway does not involve a diffusible cytosolic second messenger or a G protein. Together, these data suggest that -1 receptors are directly coupled to K ϩ channels in intracardiac neurons. Furthermore, activation of -1 receptors depresses the excitability of intracardiac neurons and is thus likely to block parasympathetic input to the heart.

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Section: Methodssupporting

confidence: 59%

Section: Methodsmentioning

confidence: 99%

σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

Zhang¹,

Cuevas²

2005

J Pharmacol Exp Ther

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“…The action potential repolarization is not affected by the Ca2+ channel blocker, Cd2+, but the magnitude and duration of the AHP are reduced in the presence of either Cd2+ or Ca2+-free external solutions [45,46]. Superfusion of Ca2+-free solutions has been reported to cause a small membrane depolarization in rat intracardiac neurons [40] and it has been suggested that IK,Ca may contribute to the resting membrane potential.…”

Section: Introductionmentioning

confidence: 99%

“…In neonatal and adult rat intracardiac neurons, the Ca2+-dependent K+ current (IK,Ca) accounts for approximately one-third of the total outward K+ current [45,46]. The action potential repolarization is not affected by the Ca2+ channel blocker, Cd2+, but the magnitude and duration of the AHP are reduced in the presence of either Cd2+ or Ca2+-free external solutions [45,46].…”

Section: Introductionmentioning

confidence: 99%

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Franciolini

Hogg

Catacuzzeno

et al. 2000

Pflügers Arch - Eur J Physiol

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The properties of single Ca2+-activated K+ (BK) channels in neonatal rat intracardiac neurons were investigated using the patch-clamp recording technique. In symmetrical 140 mM K+, the single-channel slope conductance was linear in the voltage range -60/+60 mV, and was 207±19 pS. Na+ ions were not measurably permeant through the open channel. Channel activity increased with the cytoplasmic free Ca2+ concentration ([Ca2+]i) with a Hill plot giving a halfsaturating [Ca2+] (K0.5) of 1.35 μM and slope of Ε3. The BK channel was inhibited reversibly by external tetraethylammonium (TEA) ions, charybdotoxin, and quinine and was resistant to block by 4-aminopyridine and apamin. Ionomycin (1-10 μM) increased BK channel activity in the cell-attached recording configuration. The resting activity was consistent with a [Ca2+]i <100 nM and the increased channel activity evoked by ionomycin was consistent with a rise in [Ca2+]i to ε0.3 μM. TEA (0.2-1 mM) increased the action potential duration Ε1.5-fold and reduced the amplitude and duration of the afterhyperpolarization (AHP) by 26%. Charybdotoxin (100 nM) did not significantly alter the action potential duration or AHP amplitude but reduced the AHP duration by Ε40%. Taken together, these data indicate that BK channel activation contributes to the action potential and AHP duration in rat intracardiac neurons.

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“…Interestingly, in adult rat sympathetic neurons, it has been suggested that increases in [Ca 2ϩ ] i evoked by the nonselective cholinergic agonist carbachol are not dependent on intracellular stores (Foucart et al 1995). Activation of the M1 receptor has been shown to inhibit muscarine-sensitive K ϩ currents in rat autonomic neurons (Bernheim et al 1992;Xi-Moy and Dun 1995), whereas, the M3 receptor has been reported to induce a nonselective cation current in rat dorsolateral septal neurons (Hasuo et al 1996). In contrast, stimulation of M2 and M4 receptors activate G proteins, which in turn produce cAMP stimulating the activation of protein kinase A (PKA) and phosphorylation of PKA-dependent enzymes.…”

Section: Introductionmentioning

confidence: 99%

Muscarinic and Nicotinic ACh Receptor Activation Differentially Mobilize Ca²⁺in Rat Intracardiac Ganglion Neurons

Beker

Weber

Fink

et al. 2003

Journal of Neurophysiology

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. Muscarinic and nicotinic ACh receptor activation differentially mobilize Ca 2ϩ in rat intracardiac ganglion neurons. J Neurophysiol 90: 1956-1964, 2003. First published May 21, 2003 10.1152/jn.01079.2002. The origin of intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) transients stimulated by nicotinic (nAChR) and muscarinic (mAChR) receptor activation was investigated in fura-2-loaded neonatal rat intracardiac neurons. ACh evoked [Ca 2ϩ ] i increases that were reduced to ϳ60% of control in the presence of either atropine (1 M) or mecamylamine (3 M) and to Ͻ20% in the presence of both antagonists. Removal of external Ca 2ϩ reduced ACh-induced responses to 58% of control, which was unchanged in the presence of mecamylamine but reduced to 5% of control by atropine. The nAChR-induced [Ca 2ϩ ] i response was reduced to 50% by 10 M ryanodine, whereas the mAChRinduced response was unaffected by ryanodine, suggesting that Ca 2ϩ release from ryanodine-sensitive Ca 2ϩ stores may only contribute to the nAChR-induced [Ca 2ϩ ] i responses. Perforated-patch whole cell recording at -60 mV shows that the rise in [Ca 2ϩ ] i is concomitant with slow outward currents on mAChR activation and with rapid inward currents after nAChR activation. In conclusion, different signaling pathways mediate the rise in [Ca 2ϩ ] i and membrane currents evoked by ACh binding to nicotinic and muscarinic receptors in rat intracardiac neurons.

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Potassium currents in adult rat intracardiac neurones.

Cited by 45 publications

References 42 publications

σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Muscarinic and Nicotinic ACh Receptor Activation Differentially Mobilize Ca²⁺in Rat Intracardiac Ganglion Neurons

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Potassium currents in adult rat intracardiac neurones.

Cited by 45 publications

References 42 publications

σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

σ Receptor Activation Blocks Potassium Channels and Depresses Neuroexcitability in Rat Intracardiac Neurons

Large-conductance calcium-activated potassium channels in neonatal rat intracardiac ganglion neurons

Muscarinic and Nicotinic ACh Receptor Activation Differentially Mobilize Ca2+in Rat Intracardiac Ganglion Neurons

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Muscarinic and Nicotinic ACh Receptor Activation Differentially Mobilize Ca²⁺in Rat Intracardiac Ganglion Neurons