Electrogenesis of Pacemaker Potential as Revealed by AV Nodal Experiments

1984 ◽  
pp. 97-107 ◽  
Author(s):  
H. Irisawa ◽  
A. Noma ◽  
S. Kokubun ◽  
Y. Kurachi
Keyword(s):  
Pacemaker Potential

Basal cGMP regulates the resting pacemaker potential frequency of cultured mouse colonic interstitial cells of Cajal

2014 ◽  
Vol 387 (7) ◽  
pp. 641-648 ◽  
Author(s):  
Pawan Kumar Shahi ◽  
Seok Choi ◽  
Yu Jin Jeong ◽  
Chan Guk Park ◽  
Insuk So ◽  
...  
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Pacemaker Potential ◽  
Cells Of Cajal ◽  
Potential Frequency

scholarly journals On The Mechanism of Spontaneous Impulse Generation in the Pacemaker of the Heart

1961 ◽  
Vol 45 (2) ◽  
pp. 317-330 ◽  
Author(s):  
Wolfgang Trautwein ◽  
Donald G. Kassebaum
Keyword(s):  
Sodium Current ◽  
Potassium Conductance ◽  
Rhythmic Activity ◽  
Current Strength ◽  
Heart Beat ◽  
Free Medium ◽  
Pacemaker Potential ◽  
Impulse Generation ◽  
Sodium Conductance ◽  
Voltage Dependent

Rhythmic activity in Purkinje fibers of sheep and in fibers of the rabbit sinus can be produced or enhanced when a constant depolarizing current is applied. When extracellular calcium is reduced successively, the required current strength is less, and eventually spontaneous beating occurs. These effects are believed due to an increase in steady-state sodium conductance. A significant hyperpolarization occurs in fibers of the rabbit sinus bathed in a sodium-free medium, suggesting an appreciable sodium conductance of the "resting" membrane. During diastole, there occurs a voltage-dependent and, to a smaller extent, time-dependent reduction in potassium conductance, and a pacemaker potential occurs as a result of a large resting sodium conductance. It is postulated that the mechanism underlying the spontaneous heart beat is a high resting sodium current in pacemaker tissue which acts as the generator of the heart beat when, after a regenerative repolarization, the decrease in potassium conductance during diastole reestablishes the condition of threshold.

scholarly journals Magnolia Officinalis Bark Extract Induces Depolarization of Pacemaker Potentials Through M2 and M3 Muscarinic Receptors in Cultured Murine Small Intestine Interstitial Cells of Cajal

2017 ◽  
Vol 43 (5) ◽  
pp. 1790-1802 ◽  
Author(s):  
Hyun Jung Kim ◽  
Taewon Han ◽  
Yun Tai Kim ◽  
Insuk So ◽  
Byung Joo Kim
Keyword(s):  
Receptor Antagonist ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Pacemaker Potential ◽  
Pacemaker Potentials ◽  
Magnolia Officinalis ◽  
Cells Of Cajal ◽  
Gi Motility

Background: Magnolia officinalis Rehder and EH Wilson (M. officinalis) are traditional Chinese medicines widely used for gastrointestinal (GI) tract motility disorder in Asian countries. We investigated the effects of an ethanol extract of M. officinalis (MOE) on the pacemaker potentials of cultured interstitial cells of Cajal (ICCs) in vitro and its effects on GI motor functions in vivo. Methods: We isolated ICCs from small intestines, and the whole-cell patch-clamp configuration was used to record the pacemaker potentials in cultured ICCs in vitro. Both gastric emptying (GE) and intestinal transit rates (ITRs) were investigated in normal and GI motility dysfunction (GMD) mice models in vivo. Results: MOE depolarized ICC pacemaker potentials dose-dependently. Pretreatment with methoctramine (a muscarinic M2 receptor antagonist) and 4-DAMP (a muscarinic M3 receptor antagonist) inhibited the effects of MOE on the pacemaker potential relative to treatment with MOE alone. In addition, MOE depolarized pacemaker potentials after pretreatment with Y25130 (a 5-HT3 receptor antagonist), GR113808 (a 5-HT4 receptor antagonist) or SB269970 (a 5-HT7 receptor antagonist). However, pretreatment with RS39604 (a 5-HT4 receptor antagonist) blocked MOE-induced pacemaker potential depolarizations. Intracellular GDPβS inhibited MOE-induced pacemaker potential depolarization, as did pretreatment with Ca2+ free solution or thapsigargin. In normal mice, the GE and ITR values were significantly and dose-dependently increased by MOE. In loperamide-and cisplatin-induced GE delay models, MOE administration reversed the GE deficits. The ITRs of the GMD mice were significantly reduced relative to those of normal mice, which were significantly and dose-dependently reversed by MOE. Conclusion: These results suggest that MOE dose-dependently depolarizes ICCs pacemaker potentials through M2 and M3 receptors via internal and external Ca2+ regulation through G protein pathways in vitro. Moreover, MOE increased GE and ITRs in vivo in normal and GMD mouse models. Taken together, the results of this study show that MOE have the potential for development as a gastroprokinetic agent in GI motility function.

Factors influencing motoneuron rhythmic firing: results from a voltage-clamp study

1982 ◽  
Vol 48 (4) ◽  
pp. 875-890 ◽  
Author(s):  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Firing Rate ◽  
Voltage Clamp ◽  
Sodium Current ◽  
Constant Current ◽  
Voltage Range ◽  
Pacemaker Potential ◽  
Firing Rates ◽  
Secondary Range ◽  
Rhythmic Firing ◽  
Fast Firing

1. The rhythmic firing properties of cat lumbar motoneurons were determined by intracellular injection of constant-current pulses. The activation thresholds of various membrane current components were subsequently determined in the same neurons using the technique of somatic voltage clamp. Voltage steps were employed that traversed the same voltage range as the membrane potential between rhythmic spikes (the "pacemaker potential"). 2. At fast firing rates (e.g., secondary-range firing), the pacemaker potential remains entirely within the range of voltages over which a previously described (42), persistent, inward, calcium current (Ii) is activated during voltage clamp. Thus Ii is tonically activated and counters the repolarizing, outward, potassium currents during fast firing. At slower firing rates (e.g., primary-range firing), the pacemaker potential only partially enters the voltage range where Ii is activated, and this voltage range may not be entered at all the slowest firing rates. Cells in which Ii deteriorated could not be made to fire at fast rates although they could still fire at slow rates. 3. The use of two independent intracellular microelectrodes allowed accurate measurement of the somatic voltage at which spike initiation occurred ("firing level"). In all cells, firing level increased significantly as steady firing rate increased. During a given injected-current pulse, firing level also exhibited a more moderate variation with time. 4. The variation in firing level was caused by the accommodative properties of the axon initial segment. Except at the fastest firing rates, firing level occurs at less depolarized voltages than the somatic sodium conductance threshold. In addition, somatic sodium current shows minimal inactivation over the voltage range traversed by the pacemaker potentials during slower firing rates. An inactivation of about 50% is attained during the maximum firing rate. 5. We discuss the ways by which Ii activation and thr progressive rise in firing level influence motoneuron rhythmic firing. We propose that the basic role of Ii is to aid in maintaining a linear f-I curve, especially at faster firing rates. We hypothesize that the relative balance between persistent inward and outward ionic currents plays a major role in determining the f-I curve slope among different neurons and between primary- and secondary-range firing of cat lumbar motoneurons.

Studies on bursting pacemaker potential activity in molluscan neurons. III. Effects of hormones

1975 ◽  
Vol 84 (3) ◽  
pp. 501-513 ◽  
Author(s):  
Jeffery L. Barker ◽  
Mark S. Ifshin ◽  
Harold Gainer
Keyword(s):  
Molluscan Neurons ◽  
Pacemaker Potential ◽  
Potential Activity

scholarly journals Inhibitory Synapses on Pacemaker Neurons in the Heart Ganglion of a Stomatopod, Squilla oratoria

1968 ◽  
Vol 52 (6) ◽  
pp. 908-924 ◽  
Author(s):  
Akira Watanabe ◽  
Shosaku Obara ◽  
Toyohiro Akiyama
Keyword(s):  
Membrane Potential ◽  
Nerve Stimulation ◽  
Membrane Conductance ◽  
Heart Beat ◽  
Inhibitory Synapses ◽  
Pacemaker Cell ◽  
Pacemaker Neurons ◽  
Pacemaker Potential ◽  
Steady Level ◽  
Potential Level

The pacemaker neurons of the Squilla heart ganglion are innervated from the CNS through three pairs of extrinsic nerves. One of them, the α-nerve, is inhibitory to the heart beat. The effect of α-nerve stimulation on the pacemaker potential was examined with intracellular electrodes. Without extrinsic nerve stimulation the membrane potential of the pacemaker cell fluctuated spontaneously. On application of a tetanic train of stimuli to the α-nerve the membrane potential was shifted and fixed to a steady level, which with K2SO4-filled electrodes was near the peak of hyperpolarization after a spontaneous burst, but was less negative with KCl-filled electrodes. The shift of the membrane potential was due to the summated IPSP's. By changing the level of the membrane potential with injection of the polarizing current the IPSP could be reversed in sign, and the size of the IPSP was linearly correlated with the membrane potential level. During inhibition the membrane conductance increased. The increase depended on divalent cation concentrations in the outside medium. In Ca-rich saline the IPSP was greatly enhanced. In Mg-rich saline it was suppressed. The amplitude of antidromic spikes was reduced during inhibition especially when the spike frequency was high.

In vivo Recording of Renal Pelvic Pacemaker Potential

1984 ◽  
Vol 39 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Takashi Morita ◽  
Shun Kondo ◽  
Takashi Suzuki
Keyword(s):  
Pacemaker Potential
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