Role of Voltage-Gated K+ Currents in Mediating the Regular-Spiking Phenotype of Callosal-Projecting Rat Visual Cortical Neurons

1997 ◽  
Vol 78 (5) ◽  
pp. 2321-2335 ◽  
Author(s):  
Rachel E. Locke ◽  
Jeanne M. Nerbonne
Keyword(s):  
Action Potential ◽  
Cortical Neurons ◽  
Action Potentials ◽  
Repetitive Firing ◽  
Functional Roles ◽  
Firing Rates ◽  
Voltage Gated ◽  
Firing Properties ◽  
Visual Cortical

Locke, Rachel E. and Jeanne M. Nerbonne. Role of voltage-gated K+ currents in mediating the regular-spiking phenotype of callosal-projecting rat visual cortical neurons. J. Neurophysiol. 78: 2321–2335, 1997. Whole cell current- and voltage-clamp recordings were combined to examine action potential waveforms, repetitive firing patterns, and the functional roles of voltage-gated K+ currents ( I A, I D, and I K) in identified callosal-projecting (CP) neurons from postnatal (day 7–13) rat primary visual cortex. Brief (1 ms) depolarizing current injections evoke single action potentials in CP neurons with mean ± SD ( n = 60) durations at 50 and 90% repolarization of 1.9 ± 0.5 and 5.5 ± 2.0 ms, respectively; action potential durations in individual cells are correlated inversely with peak outward current density. During prolonged threshold depolarizing current injections, CP neurons fire repetitively, and two distinct, noninterconverting “regular-spiking” firing patterns are evident: weakly adapting CP cells fire continuously, whereas strongly adapting CP cells cease firing during maintained depolarizing current injections. Action potential repolarization is faster and afterhyperpolarizations are more pronounced in strongly than in weakly adapting CP cells. In addition, input resistances are lower and plateau K+ current densities are higher in strongly than in weakly adapting CP cells. Functional studies reveal that blockade of I D reduces the latency to firing an action potential, and increases action potential durations at 50 and 90% repolarization. Blockade of I D also increases firing rates in weakly adapting cells and results in continuous firing of strongly adapting cells. After applications of millimolar concentrations of 4-aminopyridine to suppress I A (as well as block I D), action potential durations at 50 and 90% repolarization are further increased, and firing rates are accelerated over those observed when only I D is blocked. Using VClamp/CClamp and the voltage-clamp data in the preceding paper, mathematical descriptions of I A, I D, and I K are generated and a model of the electrophysiological properties of rat visual cortical CP neurons is developed. The model is used to simulate the firing properties of strongly adapting and weakly adapting CP cells and to explore the functional roles of I A, I D, and I K in shaping the waveforms of individual action potentials and controlling the repetitive firing properties of these cells.

Role of acetylcholine in induction of repetitive activity in human atrial fibers

1989 ◽  
Vol 256 (1) ◽  
pp. H74-H84
Author(s):  
Z. Y. Hou ◽  
C. I. Lin ◽  
M. Vassalle ◽  
B. N. Chiang ◽  
K. K. Cheng
Keyword(s):  
Action Potential ◽  
Muscarinic Receptor ◽  
Action Potentials ◽  
Oscillatory Potentials ◽  
Contractile Force ◽  
Intracellular Level ◽  
Transmembrane Potentials ◽  
Rebound Increase

The actions of acetylcholine and its interactions with epinephrine were studied in human atrial tissues by recording transmembrane potentials and contractile force. Acetylcholine (0.55-5.5 microM) reduced force, shortened the duration and shifted to more negative values the plateau of action potentials, abolished phase 4 depolarization, and suppressed the activity of spontaneous fibers. During the recovery, often there was a rebound increase in some parameters of the action potential and in force. Epinephrine (0.3-2.8 microM) induced oscillatory potentials and aftercontractions and acetylcholine abolished them. However, during the washout of acetylcholine in the presence of epinephrine, the oscillatory potentials and aftercontractions were larger than before acetylcholine, and repetitive activity was often induced. The inhibitory and excitatory effects of acetylcholine were mimicked by methacholine (5.1 microM) and abolished by atropine (1.5 microM). The postacetylcholine rebound was also potentiated by theophylline (0.6-2 mM) but was not blocked by propranolol (1-3.4 microM), prazosin (1 microM), and diltiazem (0.1 microM). It is concluded that in human atrial fibers acetylcholine has inhibitory as well as excitatory effects that are exaggerated in the presence of epinephrine and are mediated by the activation of the muscarinic receptor. The interaction between acetylcholine and epinephrine involves an antagonism at an intracellular level.

High Safety Factor for Action Potential Conduction Along Axons But Not Dendrites of Cultured Hippocampal and Cortical Neurons

1998 ◽  
Vol 80 (4) ◽  
pp. 2089-2101 ◽  
Author(s):  
Paul J. Mackenzie ◽  
Timothy H. Murphy
Keyword(s):  
Action Potential ◽  
Safety Factor ◽  
Cortical Neurons ◽  
Neuronal Firing ◽  
Repetitive Firing ◽  
Current Clamp ◽  
Similar Reduction ◽  
Axonal Conduction ◽  
Cultured Cortical Neurons ◽  
20 Nm

Mackenzie, Paul J. and Timothy H. Murphy. High safety factor for action potential conduction along axons but not dendrites of cultured hippocampal and cortical neurons. J. Neurophysiol. 80: 2089–2101, 1998. By using a combination of Ca2+ imaging and current-clamp recording, we previously reported that action potential (AP) conduction is reliably observed from the soma to axonal terminals in cultured cortical neurons. To extend these studies, we evaluated Ca2+ influx evoked by Na+ APs as a marker of AP conduction under conditions that are expected to lower the conduction safety factor to explore mechanisms of axonal and dendritic excitability. As expected, reducing the extracellular Na+ concentration from 150 to ∼60 mM decreased the amplitude of APs recorded in the soma but surprisingly did not influence axonal conduction, as monitored by measuring Ca2+ transients. Furthermore, reliable axonal conduction was observed in dilute (20 nM) tetrodotoxin (TTX), despite a similar reduction in AP amplitude. In contrast, the Ca2+ transient measured along dendrites was markedly reduced in low Na+, although still mediated by TTX-sensitive Na+ channels. Dendritic action-potential evoked Ca2+ transients were also markedly reduced in 20 nM TTX. These data provide further evidence that strongly excitable axons are functionally compartmentalized from weakly excitable dendrites. We conclude that modulation of Na+ currents or membrane potential by neurotransmitters or repetitive firing is more likely to influence neuronal firing before AP generation than the propagation of signals to axonal terminals. In contrast, the relatively low safety factor for back-propagating APs in dendrites would suggest a stronger effect of Na+ current modulation.

Effect of sodium deficiency of the action potential of the smooth muscle of ureter

1964 ◽  
Vol 206 (1) ◽  
pp. 205-210 ◽  
Author(s):  
Makoto Kobayashi ◽  
Hiroshi Irisawa
Keyword(s):  
Smooth Muscle ◽  
Action Potential ◽  
Action Potentials ◽  
Essential Role ◽  
Choline Chloride ◽  
Resting Potential ◽  
Sodium Deficiency ◽  
Repolarization Phase ◽  
Extracellular Sodium

Action potentials of the smooth muscle of cat ureter were studied by using ultramicroelectrodes. Among 193 penetrations, the resting potential averaged 45 mv and the amplitude of action potential 32 mv. In four instances a slight overshoot was recorded. Action potential consisted of a relatively rapid rising phase followed by a slow repolarization phase, and its duration was about 0.3 sec. Effects of sodium deficiency on action potential were studied by using three different sodium substitutes. Both the height and the rising rate of action potential decreased as the concentration of extracellular sodium was reduced, indicating that the action potential of ureter muscle can be explained on the basis of sodium theory. The duration of the action potential was prolonged when sucrose or choline chloride was used as a sodium substitute; on the other hand, it shortened when tris chloride was employed. The essential role of sodium ions in the development of the action potential in ureter muscle is discussed.

Dopamine Modulates Two Potassium Currents and Inhibits the Intrinsic Firing Properties of an Identified Motor Neuron in a Central Pattern Generator Network

1999 ◽  
Vol 81 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Peter Kloppenburg ◽  
Robert M. Levini ◽  
Ronald M. Harris-Warrick
Keyword(s):  
Action Potential ◽  
Motor Neuron ◽  
Central Pattern Generator ◽  
Action Potentials ◽  
Potassium Current ◽  
Potassium Currents ◽  
Pattern Generator ◽  
Pyloric Network ◽  
Firing Properties ◽  
Intrinsic Firing

Kloppenburg, Peter, Robert M. Levini, and Ronald M. Harris-Warrick. Dopamine modulates two potassium currents and inhibits the intrinsic firing properties of an identified motor neuron in a central pattern generator network. J. Neurophysiol. 81: 29–38, 1999. The two pyloric dilator (PD) neurons are components [along with the anterior burster (AB) neuron] of the pacemaker group of the pyloric network in the stomatogastric ganglion of the spiny lobster Panulirus interruptus. Dopamine (DA) modifies the motor pattern generated by the pyloric network, in part by exciting or inhibiting different neurons. DA inhibits the PD neuron by hyperpolarizing it and reducing its rate of firing action potentials, which leads to a phase delay of PD relative to the electrically coupled AB and a reduction in the pyloric cycle frequency. In synaptically isolated PD neurons, DA slows the rate of recovery to spike after hyperpolarization. The latency from a hyperpolarizing prestep to the first action potential is increased, and the action potential frequency as well as the total number of action potentials are decreased. When a brief (1 s) puff of DA is applied to a synaptically isolated, voltage-clamped PD neuron, a small voltage-dependent outward current is evoked, accompanied by an increase in membrane conductance. These responses are occluded by the combined presence of the potassium channel blockers 4-aminopyridine and tetraethylammonium. In voltage-clamped PD neurons, DA enhances the maximal conductance of a voltage-sensitive transient potassium current ( I A) and shifts its V act to more negative potentials without affecting its V inact. This enlarges the “window current” between the voltage activation and inactivation curves, increasing the tonically active I A near the resting potential and causing the cell to hyperpolarize. Thus DA's effect is to enhance both the transient and resting K+ currents by modulating the same channels. In addition, DA enhances the amplitude of a calcium-dependent potassium current ( I O(Ca)), but has no effect on a sustained potassium current ( I K( V)). These results suggest that DA hyperpolarizes and phase delays the activity of the PD neurons at least in part by modulating their intrinsic postinhibitory recovery properties. This modulation appears to be mediated in part by an increase of I A and I O(Ca). I A appears to be a common target of DA action in the pyloric network, but it can be enhanced or decreased in different ways by DA in different neurons.

Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus

1997 ◽  
Vol 78 (6) ◽  
pp. 3484-3488 ◽  
Author(s):  
Huanmian Chen ◽  
Nevin A. Lambert
Keyword(s):  
Calcium Channels ◽  
Action Potential ◽  
G Protein ◽  
Pyramidal Neuron ◽  
Action Potentials ◽  
Calcium Influx ◽  
G Protein Coupled Receptors ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
G Protein Coupled

Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 μM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein–mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.

scholarly journals Mechanisms of Sustained High Firing Rates in Two Classes of Vestibular Nucleus Neurons: Differential Contributions of Resurgent Na, Kv3, and BK Currents

2010 ◽  
Vol 104 (3) ◽  
pp. 1625-1634 ◽  
Author(s):  
Aryn H. Gittis ◽  
Setareh H. Moghadam ◽  
Sascha du Lac
Keyword(s):  
Action Potential ◽  
Vestibular Nucleus ◽  
Ionic Currents ◽  
Na Channel ◽  
Firing Rates ◽  
Neuronal Populations ◽  
Firing Range ◽  
Na Currents ◽  
The Difference ◽  
Firing Properties

To fire at high rates, neurons express ionic currents that work together to minimize refractory periods by ensuring that sodium channels are available for activation shortly after each action potential. Vestibular nucleus neurons operate around high baseline firing rates and encode information with bidirectional modulation of firing rates up to several hundred Hz. To determine the mechanisms that enable these neurons to sustain firing at high rates, ionic currents were measured during firing by using the action potential clamp technique in vestibular nucleus neurons acutely dissociated from transgenic mice. Although neurons from the YFP-16 line fire at rates higher than those from the GIN line, both classes of neurons express Kv3 and BK currents as well as both transient and resurgent Na currents. In the fastest firing neurons, Kv3 currents dominated repolarization at all firing rates and minimized Na channel inactivation by rapidly transitioning Na channels from the open to the closed state. In slower firing neurons, BK currents dominated repolarization at the highest firing rates and sodium channel availability was protected by a resurgent blocking mechanism. Quantitative differences in Kv3 current density across neurons and qualitative differences in immunohistochemically detected expression of Kv3 subunits could account for the difference in firing range within and across cell classes. These results demonstrate how divergent firing properties of two neuronal populations arise through the interplay of at least three ionic currents.

scholarly journals Temporal coupling of field potentials and action potentials in the neocortex

2017 ◽  
Author(s):  
Brendon O. Watson ◽  
Mingxin Ding ◽  
György Buzsáki
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Field Potential ◽  
Electromyographic Activity ◽  
Action Potential Firing ◽  
Firing Rates ◽  
Potential Firing ◽  
Temporal Coupling ◽  
Potential Activity ◽  
The Relationship

AbstractThe local field potential (LFP) is an aggregate measure of group neuronal activity and is often correlated with the action potentials of single neurons. In recent years investigators have found that action potential firing rates increase during elevations in power high-frequency band oscillations (50-200 Hz range). However action potentials also contribute to the LFP signal itself, making the spike–LFP relationship complex. Here we examine the relationship between spike rates and LFPs in varying frequency bands in rat neocortical recordings. We find that 50-180Hz oscillations correlate most consistently with high firing rates, but that other LFPs bands also carry information relating to spiking, including in some cases anti-correlations. Relatedly, we find that spiking itself and electromyographic activity contribute to LFP power in these bands. The relationship between spike rates and LFP power varies between brain states and between individual cells. Finally, we create an improved oscillation-based predictor of action potential activity by specifically utilizing information from across the entire recorded frequency spectrum of LFP. The findings illustrate both caveats and improvements to be taken into account in attempts to infer spiking activity from LFP.

scholarly journals Dendritic Voltage-Gated Ion Channels Regulate the Action Potential Firing Mode of Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 82 (4) ◽  
pp. 1895-1901 ◽  
Author(s):  
Jeffrey C. Magee ◽  
Michael Carruth
Keyword(s):  
Ion Channels ◽  
Action Potential ◽  
Large Amplitude ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Burst Firing ◽  
Voltage Gated ◽  
Ca1 Pyramidal Neurons ◽  
Firing Mode ◽  
Voltage Gated Ion Channels

The role of dendritic voltage-gated ion channels in the generation of action potential bursting was investigated using whole cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons located in hippocampal slices of adult rats. Under control conditions somatic current injections evoked single action potentials that were associated with an afterhyperpolarization (AHP). After localized application of 4-aminopyridine (4-AP) to the distal apical dendritic arborization, the same current injections resulted in the generation of an afterdepolarization (ADP) and multiple action potentials. This burst firing was not observed after localized application of 4-AP to the soma/proximal dendrites. The dendritic 4-AP application allowed large-amplitude Na+-dependent action potentials, which were prolonged in duration, to backpropagate into the distal apical dendrites. No change in action potential backpropagation was seen with proximal 4-AP application. Both the ADP and action potential bursting could be inhibited by the bath application of nonspecific concentrations of divalent Ca2+ channel blockers (NiCl and CdCl). Ca2+ channel blockade also reduced the dendritic action potential duration without significantly affecting spike amplitude. Low concentrations of TTX (10–50 nM) also reduced the ability of the CA1 neurons to fire in the busting mode. This effect was found to be the result of an inhibition of backpropagating dendritic action potentials and could be overcome through the coordinated injection of transient, large-amplitude depolarizing current into the dendrite. Dendritic current injections were able to restore the burst firing mode (represented as a large ADP) even in the presence of high concentrations of TTX (300–500 μM). These data suggest the role of dendritic Na+ channels in bursting is to allow somatic/axonal action potentials to backpropagate into the dendrites where they then activate dendritic Ca2+ channels. Although it appears that most Ca2+ channel subtypes are important in burst generation, blockade of T- and R-type Ca2+ channels by NiCl (75 μM) inhibited action potential bursting to a greater extent than L-channel (10 μM nimodipine) or N-, P/Q-type (1 μM ω-conotoxin MVIIC) Ca2+ channel blockade. This suggest that the Ni-sensitive voltage-gated Ca2+ channels have the most important role in action potential burst generation. In summary, these data suggest that the activation of dendritic voltage-gated Ca2+ channels, by large-amplitude backpropagating spikes, provides a prolonged inward current that is capable of generating an ADP and burst of multiple action potentials in the soma of CA1 pyramidal neurons. Dendritic voltage-gated ion channels profoundly regulate the processing and storage of incoming information in CA1 pyramidal neurons by modulating the action potential firing mode from single spiking to burst firing.

scholarly journals The modulation of two motor behaviors by persistent sodium currents in Xenopus laevis tadpoles

2017 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Erik Svensson ◽  
Hugo Jeffreys ◽  
Wen-Chang Li
Keyword(s):  
Action Potentials ◽  
Sodium Current ◽  
Repetitive Firing ◽  
Sodium Currents ◽  
Spinal Neurons ◽  
Motor Behaviors ◽  
Low Concentrations ◽  
Descending Interneurons ◽  
Lateral Sclerosis

Persistent sodium currents ( INaP) are common in neuronal circuitries and have been implicated in several diseases, such as amyotrophic lateral sclerosis (ALS) and epilepsy. However, the role of INaP in the regulation of specific behaviors is still poorly understood. In this study we have characterized INaP and investigated its role in the swimming and struggling behavior of Xenopus tadpoles. INaP was identified in three groups of neurons, namely, sensory Rohon-Beard neurons (RB neurons), descending interneurons (dINs), and non-dINs (neurons rhythmically active in swimming). All groups of neurons expressed INaP, but the currents differed in decay time constants, amplitudes, and the membrane potential at which INaP peaked. Low concentrations (1 µM) of the INaP blocker riluzole blocked INaP ~30% and decreased the excitability of the three neuron groups without affecting spike amplitudes or cellular input resistances. Riluzole reduced the number of rebound spikes in dINs and depressed repetitive firing in RB neurons and non-dINs. At the behavior level, riluzole at 1 µM shortened fictive swimming episodes. It also reduced the number of action potentials neurons fired on each struggling cycle. The results show that INaP may play important modulatory roles in motor behaviors. NEW & NOTEWORTHY We have characterized persistent sodium currents in three groups of spinal neurons and their role in shaping spiking activity in the Xenopus tadpole. We then attempted to evaluate the role of persistent sodium currents in regulating tadpole swimming and struggling motor outputs by using low concentrations of the persistent sodium current antagonist riluzole.

Electrophysiological analysis of the neurotoxic action of a funnel-web spider toxin, delta-atracotoxin-HV1a, on insect voltage-gated Na+ channels

2001 ◽  
Vol 204 (4) ◽  
pp. 711-721 ◽  
Author(s):  
F. Grolleau ◽  
M. Stankiewicz ◽  
L. Birinyi-Strachan ◽  
X.H. Wang ◽  
G.M. Nicholson ◽  
...  
Keyword(s):  
Voltage Clamp ◽  
Action Potentials ◽  
Periplaneta Americana ◽  
Repetitive Firing ◽  
Na Channel ◽  
Na Channels ◽  
Patch Clamp Technique ◽  
Voltage Gated ◽  
Web Spider ◽  
Channel Inactivation

The effects of delta-ACTX-Hv1a, purified from the venom of the funnel-web spider Hadronyche versuta, were studied on the isolated giant axon and dorsal unpaired median (DUM) neurones of the cockroach Periplaneta americana under current- and voltage-clamp conditions using the double oil-gap technique for single axons and the patch-clamp technique for neurones. In parallel, the effects of the toxin were investigated on the excitability of rat dorsal root ganglion (DRG) neurones. In both DRG and DUM neurones, delta-ACTX-Hv1a induced spontaneous repetitive firing accompanied by plateau potentials. However, in the case of DUM neurones, plateau action potentials were facilitated when the membrane was artificially hyperpolarized. In cockroach giant axons, delta-ACTX-Hv1a also produced plateau action potentials, but only when the membrane was pre-treated with 3–4 diaminopyridine. Under voltage-clamp conditions, delta-ACTX-Hv1a specifically affected voltage-gated Na+ channels in both axons and DUM neurones. Both the current/voltage and conductance/voltage curves of the delta-ACTX-Hv1a-modified inward current were shifted 10 mV to the left of control curves. In the presence of delta-ACTX-Hv1a, steady-state Na+ channel inactivation became incomplete, causing the appearance of a non-inactivating component at potentials more positive than −40 mV. The amplitude of this non-inactivating component was dependent on the holding potential. From this study, it is concluded that, in insect neurones, delta-ACTX-Hv1a mainly affects Na+ channel inactivation by a mechanism that differs slightly from that of scorpion alpha-toxins.

Sign in / Sign up

Export Citation Format

Share Document