Different types of ganglion cell in the cardiac plexus of guinea‐pigs.

Edwards, Frank; Hirst, G. D. S.; Klemm, Megan F; Steele, Penelope A.

doi:10.1113/jphysiol.1995.sp020825

Cited by 105 publications

(125 citation statements)

References 38 publications

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“…The mean AHP amplitude was -12.6±0.5 mV (n=28) and reversed at approximately -90 mV, close to the K+ equilibrium potential. The duration of the AHP was highly variable ranging from approximately 50 to 250 ms, reflecting the heterogeneity of the intracardiac ganglion neuron population [2,13,40]. Apamin (1 μM, n=4), iberiotoxin (100 nM, n=6) and ChTX (100 nM, n=6) had no significant effects on the amplitude or duration of the action potential.…”

Section: Bk Channel Contribution To the Action Potential And Ahpmentioning

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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Section: Bk Channel Contribution To the Action Potential And Ahpmentioning

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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“…Individual neurons were used for an experiment if the membrane potential was Ϫ40 mV or below and they produced action potentials with an overshoot of at least 20 mV. The neurons were identified as parasympathetic postganglionic neurons by their morphology (ϳ30 m in diameter) and their basic electrical properties relative to previous studies (6,7,16).…”

Section: Methodsmentioning

confidence: 99%

Modulation of guinea pig intrinsic cardiac neurons by prostaglandins

Jelson

DeMasi

Sager

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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vation of cardiac mast cells has been shown to alter parasympathetic neuronal function via the activation of histamine receptors. The present study examined the ability of prostaglandins to alter the activity of guinea pig intracardiac neurons. Intracellular voltage recordings from whole mounts of the cardiac plexus showed that antigen-mediated mast cell degranulation produces an attenuation of the afterhyperpolarization (AHP), which was prevented by the phospholipase A2 inhibitor 5,8,11,14-eicosatetraynoic acid. Exogenous application of either PGD2 or PGE2 produced a biphasic change in the membrane potential and an inhibition of both AHP amplitude and duration. Examination of prostanoid receptors using bath perfusions (1 M PGE2 and PGD2), specific agonists (BW245C, sulprostone, and butaprost), and antagonists (AH6809 and SC19220) found evidence for both the PGE2-specific EP2 and EP3 receptors, but not for EP1 or the PGD2-specific prostanoid (DP) receptors. Sulprostone was able to mimic the PGE2 responses in some cells, but not in all PGE2-sensitive cells. Butaprost was able to mimic the PGinduced hyperpolarization in some cells, but did not alter the AHP. Inhibition of specific potassium channels with either TEA, charybdotoxin, or apamin showed that neither TEA nor charybdotoxin could prevent the PGE2-induced AHP attenuation. Apamin alone inhibited AHP duration, with PGs having no further effect in these cells. These results demonstrate that guinea pig intracardiac neurons can be modulated by PG, most likely through either EP2, EP3, or potentially EP4 receptors, and this response is due, at least in part, to a reduction in small-conductance KCa currents.

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“…Moreover, the authors demonstrated the presence of three cell subpopulations varying in neurochemical properties. Edwards et al [15], on the other hand, differentiated three neuron types in the cardiac ganglia of guinea pigs, varying in electrophysiological properties. The first type are the so-called S-cells, in which action potential is caused by short hyperpolarisation, while in types 2 and 3, the potential is created due to prolonged hyperpolarisation.…”

Section: Morphology Of Cardiac Gangliamentioning

confidence: 99%