Contribution of individual ionic currents to activity of a model stomatogastric ganglion neuron

1992 ◽  
Vol 67 (2) ◽  
pp. 341-349 ◽  
Author(s):  
J. Golowasch ◽  
F. Buchholtz ◽  
I. R. Epstein ◽  
E. Marder
Keyword(s):  
Action Potential ◽  
Model Neuron ◽  
Outward Current ◽  
Rhythmic Activity ◽  
Stomatogastric Ganglion ◽  
Delayed Rectifier ◽  
Maximal Conductance ◽  
Action Potential Frequency ◽  
Potential Frequency

1. The behavior of the mathematical model for the lateral pyloric (LP) neuron of the crustacean stomatogastric ganglion (STG) developed in the previous paper was further studied. 2. The action of proctolin, a neuromodulatory peptide that acts directly on the LP neuron, was modeled. The effect of the proctolin-activated current (iproc) on the model neuron mimics the effects of proctolin on the isolated biological LP neuron. The depolarization and increased frequency of firing seen when iproc is activated are associated with changes in the relative contributions of the delayed rectifier (id) and the Ca(2+)-activated outward current (io(Ca] to the repolarization phase of the action potential. 3. The effects of turning off the A-current (iA) in the model were compared with those obtained by pharmacologically blocking iA in the biological neuron. iA appears to regulate action-potential frequency as well as postinhibitory rebound activity. 4. The role of iA on the rhythmic activity of the cell was studied by modifying several of its parameters while periodically activating a simulated synaptically activated conductance, isyn. 5. The effects of manipulations of the maximal conductances (g) for id and io(Ca) were studied. id strongly influences action-potential frequency, whereas io(Ca) strongly influences action-potential duration. 6. Modifications of the maximal conductance of the inward Ca2+ current (iCa) were compared with the effects of blocking iCa in the real cell. 7. The role of the hyperpolarization-activated inward current (ih) during ongoing rhythmic activity was assessed by periodically activating isyn while modifying ih.

scholarly journals MOTOR NEURONES OF THE CRAYFISH WALKING SYSTEM POSSESS TEA+-REVEALED REGENERATIVE ELECTRICAL PROPERTIES

1994 ◽  
Vol 188 (1) ◽  
pp. 339-345
Author(s):  
D Cattaert ◽  
A Araque ◽  
W Buno ◽  
F Clarac
Keyword(s):  
Membrane Potential ◽  
Outward Current ◽  
Rhythmic Activity ◽  
Input Resistance ◽  
Stomatogastric Ganglion ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Muscarinic Agonist ◽  
M Current ◽  
Motor Neurones

In crustaceans, some motor neurones (MNs) have been shown to be part of the central pattern generator in the stomatogastric system (Harris-Warrick et al. 1992; Moulins, 1990), the swimmeret system (Heitler, 1978) or the walking system (Chrachri and Clarac, 1990). These MNs induce changes in the central rhythm when depolarized and are conditional oscillators in the stomatogastric ganglion. Moreover, in the walking system, rhythmic activity can be triggered by muscarinic cholinergic agonists (Chrachri and Clarac, 1987). We have recently analyzed the role of muscarinic receptors in crayfish walking leg MNs (D. Cattaert and A. Araque, in preparation) and demonstrated that oxotremorine, a muscarinic agonist, evoked long-lasting depolarizing responses associated with an increased input resistance. The outward current blocked by oxotremorine is likely to be carried by K+, as is the case for the M current (IM) in vertebrates (Brown and Adams, 1980). In most neurones, K+ conductances play a principal role in maintaining the membrane potential at rest: for example, IM is active at the resting membrane potential, thus contributing to its maintenance, and the 'delayed-rectifier' (IK) assists the fast repolarization after an action potential. Some K+ conductances are Ca2+-dependent (IK,Ca) and are activated by an increase in internal Ca2+ concentration. In such cases, Ca2+ currents may result in hyperpolarization of the neurone through activation of IK,Ca. In opposition to these K+ currents, the direct effect of Na+ and Ca2+ conductances is to depolarize the neurone. For example, the persistant Na+ current (INap) that is responsible for the slow subthreshold depolarization termed slow pre-potentials (Gestrelius et al. 1983; Leung and Yim, 1991) participates in the formation of pacemaker depolarization (Barrio et al. 1991) and generates plateau-type responses in control conditions (Barrio et al. 1991; Llinas and Sugimori, 1980). Similarly Ca2+ or non-specific (Na+/Ca2+) conductances generate such events in Aplysia californica burster neurones (Adams and Benson, 1985), crustacean cardiac ganglion (Tazaki and Cooke, 1990), insect neurones (Hancox and Pitman, 1991) and crustacean stomatogastric ganglion (Kiehn and Harris-Warrick, 1992). Since crustacean MNs can participate in rhythm production, such depolarizing conductances may exist in most of them and may contribute to the long-lasting MN depolarizations and spike bursts present during locomotion.

Characterization and functional consequences of delayed rectifier current transient in ventricular repolarization

2000 ◽  
Vol 278 (3) ◽  
pp. H806-H817 ◽  
Author(s):  
Gary A. Gintant
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Inward Rectifier ◽  
Ventricular Repolarization ◽  
Delayed Rectifier ◽  
Voltage Range ◽  
Delayed Rectifier Current ◽  
Recovery From Inactivation ◽  
Voltage Dependent

Although inactivation of the rapidly activating delayed rectifier current ( I Kr) limits outward current on depolarization, the role of I Kr (and recovery from inactivation) during repolarization is uncertain. To characterize I Krduring ventricular repolarization (and compare with the inward rectifier current, I K1), voltage-clamp waveforms simulating the action potential were applied to canine ventricular, atrial, and Purkinje myocytes. In ventricular myocytes, I Kr was minimal at plateau potentials but transiently increased during repolarizing ramps. The I Kr transient was unaffected by repolarization rate and maximal after 150-ms depolarizations (+25 mV). Action potential clamps revealed the I Kr transient terminating the plateau. Although peak I Kr transient density was relatively uniform among myocytes, potentials characterizing the peak transients were widely dispersed. In contrast, peak inward rectifier current ( I K1) density during repolarization was dispersed, whereas potentials characterizing I K1 defined a narrower (more negative) voltage range. In summary, rapidly activating I Kr provides a delayed voltage-dependent (and functionally time-independent) outward transient during ventricular repolarization, consistent with rapid recovery from inactivation. The heterogeneous voltage dependence of I Kr provides a novel means for modulating the contribution of this current during repolarization.

scholarly journals Lipopolysaccharide prolongs action potential duration in HL-1 mouse cardiomyocytes

2012 ◽  
Vol 303 (8) ◽  
pp. C825-C833 ◽  
Author(s):  
Robert Wondergem ◽  
Bridget M. Graves ◽  
Chuanfu Li ◽  
David L. Williams
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Salmonella Enteritidis ◽  
Time Course ◽  
Outward Current ◽  
Cell Voltage ◽  
Delayed Rectifier ◽  
Maximal Effect ◽  
Cellular Mechanisms ◽  
Whole Cell

Sepsis has deleterious effects on cardiac function including reduced contractility. We have shown previously that lipopolysaccharides (LPS) directly affect HL-1 cardiac myocytes by inhibiting Ca2+ regulation and by impairing pacemaker “funny” current, If. We now explore further cellular mechanisms whereby LPS inhibits excitability in HL-1 cells. LPS (1 μg/ml) derived from Salmonella enteritidis decreased rate of firing of spontaneous action potentials in HL-1 cells, and it increased their pacemaker potential durations and decreased their rates of depolarization, all measured by whole cell current clamp. LPS also increased action potential durations and decreased their amplitude in cells paced at 1 Hz with 0.1 nA, and 20 min were necessary for maximal effect. LPS decreased the amplitude of a rapidly inactivating inward current attributed to Na+ and of an outward current attributed to K+; both were measured by whole cell voltage clamp. The K+ currents displayed a resurgent outward tail current, which is characteristic of the rapid delayed-rectifier K+ current, IKr. LPS accordingly reduced outward currents measured with pipette Cs+ substituted for K+ to isolate IKr. E-4031 (1 μM) markedly inhibited IKr in HL-1 cells and also increased action potential duration; however, the direct effects of E-4031 occurred minutes faster than the slow effects of LPS. We conclude that LPS increases action potential duration in HL-1 mouse cardiomyocytes by inhibition of IKr and decreases their rate of firing by inhibition of INa. This protracted time course points toward an intermediary metabolic event, which either decreases available mouse ether-a-go-go (mERG) and Na+ channels or potentiates their inactivation.

Neurotransmitter release from high-frequency stimulation of the subthalamic nucleus

2004 ◽  
Vol 101 (3) ◽  
pp. 511-517 ◽  
Author(s):  
Kendall H. Lee ◽  
Su-Youne Chang ◽  
David W. Roberts ◽  
Uhnoh Kim
Keyword(s):  
Action Potential ◽  
High Frequency ◽  
Neurotransmitter Release ◽  
High Frequency Stimulation ◽  
Content Type ◽  
Action Potential Frequency ◽  
Frequency Stimulation ◽  
Potential Frequency ◽  
Fine Print ◽  
Stimulation Of

Object. High-frequency stimulation (HFS) delivered through implanted electrodes in the subthalamic nucleus (STN) has become an established treatment for Parkinson disease (PD). The precise mechanism of action of deep brain stimulation (DBS) in the STN is unknown, however. In the present study, the authors tested the hypothesis that HFS within the STN changes neuronal action potential firing rates during the stimulation period by modifying neurotransmitter release. Methods. Intracellular electrophysiological recordings were obtained using sharp electrodes in rat STN neurons in an in vitro slice preparation. A concentric bipolar stimulating electrode was placed in the STN slice, and electrical stimulation (pulse width 50–100 µsec, duration 100–2000 µsec, amplitude 10–500 µA, and frequency 10–200 Hz) was delivered while simultaneously obtaining intracellular recordings from an STN neuron. High-frequency stimulation of the STN either generated excitatory postsynaptic potentials (EPSPs) and increased the action potential frequency or it generated inhibitory postsynaptic potentials and decreased the action potential frequency of neurons within the STN. These effects were blocked after antagonists to glutamate and γ-aminobutyric acid were applied to the tissue slice, indicating that HFS resulted in the release of neurotransmitters. Intracellular recordings from substantia nigra pars compacta (SNc) dopaminergic neurons during HFS of the STN revealed increased generation of EPSPs and increased frequency of action potentials in SNc neurons. Conclusions. During HFS of STN neurons the mechanism of DBS may involve the release of neurotransmitters rather than the primary electrogenic inhibition of neurons.

Postnatal development has a marked effect on ventricular repolarization in mice

2007 ◽  
Vol 293 (4) ◽  
pp. H2168-H2177 ◽  
Author(s):  
Scott A. Grandy ◽  
Véronique Trépanier-Boulay ◽  
Céline Fiset
Keyword(s):  
Postnatal Development ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Ventricular Repolarization ◽  
Delayed Rectifier ◽  
Transient Outward Current ◽  
Cd1 Mice ◽  
The Individual ◽  
Immature Heart

To better understand the mechanisms that underlie cardiac repolarization abnormalities in the immature heart, this study characterized and compared K+ currents in mouse ventricular myocytes from day 1, day 7, day 20, and adult CD1 mice to determine the effects of postnatal development on ventricular repolarization. Current- and patch-clamp techniques were used to examine action potentials and the K+ currents underlying repolarization in isolated myocytes. RT-PCR was used to quantify mRNA expression for the K+ channels of interest. This study found that action potential duration (APD) decreased as age increased, with the shortest APDs observed in adult myocytes. This study also showed that K+ currents and the mRNA relative abundance for the various K+ channels were significantly greater in adult myocytes compared with day 1 myocytes. Examination of the individual components of total K+ current revealed that the inward rectifier K+ current ( IK1) developed by day 7, both the Ca2+-independent transient outward current ( Ito) and the steady-state outward K+ current ( Iss) developed by day 20, and the ultrarapid delayed rectifier K+ current ( IKur) did not fully develop until the mouse reached maturity. Interestingly, the increase in IKur was not associated with a decrease in APD. Comparison of atrial and ventricular K+ currents showed that Ito and IKur density were significantly greater in day 7, day 20, and adult myocytes compared with age-matched atrial cells. Overall, it appears that, in mouse ventricle, developmental changes in APD are likely attributable to increases in Ito, Iss, and IK1, whereas the role of IKur during postnatal development appears to be less critical to APD.

Glucose, insulin, and leptin signaling pathways modulate nitric oxide synthesis in glucose-inhibited neurons in the ventromedial hypothalamus

2007 ◽  
Vol 292 (4) ◽  
pp. R1418-R1428 ◽  
Author(s):  
Debra D. Canabal ◽  
Zhentao Song ◽  
Joseph G. Potian ◽  
Annie Beuve ◽  
Joseph J. McArdle ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Action Potential ◽  
Insulin Signaling ◽  
Ventromedial Hypothalamus ◽  
Glucose Sensing ◽  
No Production ◽  
Obesity And Diabetes ◽  
Action Potential Frequency ◽  
Extracellular Glucose ◽  
Potential Frequency

Glucose-sensing neurons in the ventromedial hypothalamus (VMH) are involved in the regulation of glucose homeostasis. Glucose-sensing neurons alter their action potential frequency in response to physiological changes in extracellular glucose, insulin, and leptin. Glucose-excited neurons decrease, whereas glucose-inhibited (GI) neurons increase, their action potential frequency when extracellular glucose is reduced. Central nitric oxide (NO) synthesis is regulated by changes in local fuel availability, as well as insulin and leptin. NO is involved in the regulation of food intake and is altered in obesity and diabetes. Thus this study tests the hypothesis that NO synthesis is a site of convergence for glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. With the use of the NO-sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein in conjunction with the membrane potential-sensitive dye fluorometric imaging plate reader, we found that glucose and leptin suppress, whereas insulin stimulates neuronal nitric oxide synthase (nNOS)-dependent NO production in cultured VMH GI neurons. The effects of glucose and leptin were mediated by suppression of AMP-activated protein kinase (AMPK). The AMPK activator 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) increased both NO production and neuronal activity in GI neurons. In contrast, the effects of insulin on NO production were blocked by the phosphoinositide 3-kinase inhibitors wortmannin and LY-294002. Furthermore, decreased glucose, insulin, and AICAR increase the phosphorylation of VMH nNOS, whereas leptin decreases it. Finally, VMH neurons express soluble guanylyl cyclase, a downstream mediator of NO signaling. Thus NO may mediate, in part, glucose, leptin, and insulin signaling in VMH glucose-sensing neurons.

scholarly journals Passive properties and membrane currents of canine ventricular myocytes.

1987 ◽  
Vol 90 (5) ◽  
pp. 671-701 ◽  
Author(s):  
G N Tseng ◽  
R B Robinson ◽  
B F Hoffman
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Cardiac Cells ◽  
Membrane Currents ◽  
Membrane Properties ◽  
Delayed Rectifier ◽  
Transient Outward Current ◽  
Fast Kinetics

The membrane potential and membrane currents of single canine ventricular myocytes were studied using either single microelectrodes or suction pipettes. The myocytes displayed passive membrane properties and an action potential configuration similar to those described for multicellular dog ventricular tissue. As for other cardiac cells, in canine ventricular myocytes: (a) an inward rectifier current plays an important role in determining the resting membrane potential and repolarization rate; (b) a tetrodotoxin-sensitive Na current helps maintain the action potential plateau; and (c) the Ca current has fast kinetics and a large amplitude. Unexpected findings were the following: (a) in approximately half of the myocytes, there is a transient outward current composed of two components, one blocked by 4-aminopyridine and the other by Mn or caffeine; (b) there is clearly a time-dependent outward current (delayed rectifier current) that contributes to repolarization; and (c) the relationship of maximum upstroke velocity of phase 0 to membrane potential is more positive and steeper than that observed in cardiac tissues from Purkinje fibers.

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