Is the frequency dependent shortening of the action potential caused by an extracellular potassium accumulation?

1967 ◽  
Vol 257 (3) ◽  
pp. 323-324 ◽  
Author(s):  
M. Reiter ◽  
F. J. Stickel
Keyword(s):  
Action Potential ◽  
Extracellular Potassium ◽  
Potassium Accumulation ◽  
Frequency Dependent

scholarly journals Activity-mediated accumulation of potassium induces a switch in firing pattern and neuronal excitability type

2021 ◽  
Vol 17 (5) ◽  
pp. e1008510
Author(s):  
Susana Andrea Contreras ◽  
Jan-Hendrik Schleimer ◽  
Allan T. Gulledge ◽  
Susanne Schreiber
Keyword(s):  
Action Potential ◽  
Neuronal Activity ◽  
Brain State ◽  
Extracellular Potassium ◽  
Action Potential Generation ◽  
Potential Generation ◽  
Potassium Accumulation ◽  
Voltage Dynamics ◽  
The Impact ◽  
Spiking Activity

During normal neuronal activity, ionic concentration gradients across a neuron’s membrane are often assumed to be stable. Prolonged spiking activity, however, can reduce transmembrane gradients and affect voltage dynamics. Based on mathematical modeling, we investigated the impact of neuronal activity on ionic concentrations and, consequently, the dynamics of action potential generation. We find that intense spiking activity on the order of a second suffices to induce changes in ionic reversal potentials and to consistently induce a switch from a regular to an intermittent firing mode. This transition is caused by a qualitative alteration in the system’s voltage dynamics, mathematically corresponding to a co-dimension-two bifurcation from a saddle-node on invariant cycle (SNIC) to a homoclinic orbit bifurcation (HOM). Our electrophysiological recordings in mouse cortical pyramidal neurons confirm the changes in action potential dynamics predicted by the models: (i) activity-dependent increases in intracellular sodium concentration directly reduce action potential amplitudes, an effect typically attributed solely to sodium channel inactivation; (ii) extracellular potassium accumulation switches action potential generation from tonic firing to intermittently interrupted output. Thus, individual neurons may respond very differently to the same input stimuli, depending on their recent patterns of activity and/or the current brain-state.

Preceding Stimulus Frequency-Dependent Potentiation of the Postrest Shortening of the Action Potential Duration in Rabbits.

2000 ◽  
Vol 41 (4) ◽  
pp. 481-492
Author(s):  
Naohiko Takahashi ◽  
Morio Ito ◽  
Shuji Ishida ◽  
Takao Fujino ◽  
Mikiko Nakagawa ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Stimulus Frequency ◽  
Frequency Dependent ◽  
Preceding Stimulus

scholarly journals Potassium diffusive coupling in neural networks

2010 ◽  
Vol 365 (1551) ◽  
pp. 2347-2362 ◽  
Author(s):  
Dominique M. Durand ◽  
Eun-Hyoung Park ◽  
Alicia L. Jensen
Keyword(s):  
Neural Networks ◽  
Neural Activity ◽  
Neuronal Excitability ◽  
Epileptiform Activity ◽  
Lateral Diffusion ◽  
Normal Activity ◽  
Ionic Concentration ◽  
Extracellular Potassium ◽  
Potassium Accumulation ◽  
Diffusive Coupling

Conventional neural networks are characterized by many neurons coupled together through synapses. The activity, synchronization, plasticity and excitability of the network are then controlled by its synaptic connectivity. Neurons are surrounded by an extracellular space whereby fluctuations in specific ionic concentration can modulate neuronal excitability. Extracellular concentrations of potassium ([K + ] o ) can generate neuronal hyperexcitability. Yet, after many years of research, it is still unknown whether an elevation of potassium is the cause or the result of the generation, propagation and synchronization of epileptiform activity. An elevation of potassium in neural tissue can be characterized by dispersion (global elevation of potassium) and lateral diffusion (local spatial gradients). Both experimental and computational studies have shown that lateral diffusion is involved in the generation and the propagation of neural activity in diffusively coupled networks. Therefore, diffusion-based coupling by potassium can play an important role in neural networks and it is reviewed in four sections. Section 2 shows that potassium diffusion is responsible for the synchronization of activity across a mechanical cut in the tissue. A computer model of diffusive coupling shows that potassium diffusion can mediate communication between cells and generate abnormal and/or periodic activity in small (§3) and in large networks of cells (§4). Finally, in §5, a study of the role of extracellular potassium in the propagation of axonal signals shows that elevated potassium concentration can block the propagation of neural activity in axonal pathways. Taken together, these results indicate that potassium accumulation and diffusion can interfere with normal activity and generate abnormal activity in neural networks.

Action potential propagation through embryonic dorsal root ganglion cells in culture. II. Decrease of conduction reliability during repetitive stimulation

1994 ◽  
Vol 72 (2) ◽  
pp. 634-643 ◽  
Author(s):  
C. Luscher ◽  
J. Streit ◽  
P. Lipp ◽  
H. R. Luscher
Keyword(s):  
Dorsal Root Ganglion ◽  
Action Potential ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Channel Blocker ◽  
Extracellular Calcium ◽  
Repetitive Stimulation ◽  
Calcium Currents ◽  
Double Pulse ◽  
Extracellular Potassium

1. The reliability of the propagation of action potentials (AP) through dorsal root ganglion (DRG) cells in embryonic slice cultures was investigated during repetitive stimulation at 1–20 Hz. Membrane potentials of DRG cells were recorded intracellularly while the axons were stimulated by an extracellular electrode. 2. In analogy to the double-pulse experiments reported previously, either one or two types of propagation failures were recorded during repetitive stimulation, depending on the cell morphology. In contrast to the double-pulse experiments, the failures appeared at longer interpulse intervals and usually only after several tens of stimuli with reliable propagation. 3. In the period with reliable propagation before the failures, a decrease in the conduction velocity and in the amplitude of the afterhyperpolarization (AHP), an increase in the total membrane conductance, and the disappearance of the action potential “shoulder” were observed. 4. The reliability of conduction during repetitive stimulation was improved by lowering the extracellular calcium concentration or by replacing the extracellular calcium by strontium. The reliability of conduction decreased by the application of cadmium, a calcium channel blocker, 4-amino pyridine, a fast potassium channel blocker, or apamin or muscarine, the blockers of calcium-dependent potassium channels. The reliability of conduction was not effected by blocking the sodium potassium pump with ouabain or by replacing extracellular sodium with lithium. 5. In the period with reliable propagation cadmium, apamin, and muscarine reduced the amplitude of the AHP. The shoulder of the action potential was more pronounced and not sensitive to repetitive stimulation when extracellular calcium was replaced by strontium. It disappeared when cadmium was applied. 6. In DRG somata changes of the intracellular Ca2+ concentration were monitored by measuring the fluorescence of the Ca2+ indicator Fluo-3 with a laser-scanning confocal microscope. During repetitive stimulation, an accumulation of intracellular calcium occurred that recovered very slowly (tens of seconds) after the AP trains. 7. Computer model simulations performed in analogy to the experimental protocols produced conduction failures during repetitive stimulation only when the calcium currents during the APs were reduced. 8. From these findings it is concluded that conduction failures during repetitive stimulation are dependent on an accumulation of intracellular calcium leading to an inactivation of calcium currents, combined with small contributions of an accumulation of extracellular potassium and a summation of slow potassium conductances.

AN ANALYSIS OF CONTROL OF THE VENTRICLE OF THE MOLLUSC MERCENARIA MERCENARIA

1993 ◽  
Vol 179 (1) ◽  
pp. 47-61
Author(s):  
C. L. Devlin
Keyword(s):  
Action Potential ◽  
Mercenaria Mercenaria ◽  
Lanthanum Chloride ◽  
Cardiac Action Potential ◽  
Extracellular Potassium ◽  
Plateau Phase ◽  
Progressive Reduction ◽  
Barium Ions ◽  
Cardiac Action ◽  
Ionophore Monensin

During spontaneous beating (autorhythmicity) in the bivalve ventricle, the cardiac action potential (AP) was generated by calcium (Ca2+) and sodium (Na+) influx. The initial fast rising phase (the ‘spike’) of the cardiac AP was dependent on extracellular Ca2+ concentration, whereas the slow plateau phase was Na+-dependent. The initial fast rising phase of the cardiac AP was abolished by treatment with a Ca2+-free saline or inorganic Ca2+ entry blockers, such as lanthanum chloride or cobalt. Conversely, this fast rising phase of the AP was potentiated by treatment with barium ions, the dihydropyridine-sensitive Ca2+ channel agonist Bay K 8644 or, unexpectedly, by the organic Ca2+ entry blocker diltiazem. The force of systolic beating was directly proportional to the amplitude of the fast rising phase of the cardiac AP. The Ca2+-dependent, fast rising phase of the AP was modulated by the level of extracellular Na+. Both the amplitude of the fast rising phase of the AP and coupled systolic force were increased by progressive reduction of extracellular Na+ concentration. The slow plateau phase was abolished by treatment with a Na+-free saline and potentiated by the Na+ ionophore monensin. The size of the Na+-dependent plateau was modulated by the level of extracellular Ca2+. When extracellular Ca2+ was removed from the bathing saline, both the amplitude and duration of the plateau phase were increased. Conversely, restoring extracellular Ca2+ to physiological levels decreased the size of the Na+-dependent plateau. Autorhythmicity was dependent on the level of extracellular potassium. In the absence of K+, neither a Ca2+-dependent fast rising phase nor a Na+-dependent plateau phase was recorded.

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