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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The success or failure of the propagation of electrical activity in cardiac tissue is dependent on both cellular membrane characteristics and intercellular coupling properties. This paper considers a linear arrangement of individual bullfrog atrial cells that are resistively coupled end to end to form a cylindrical strand. The strand, in turn, is encased by an endothelial sheath that provides a restricted extracellular space and an ion diffusion barrier to the outer bathing medium. This encased strand serves as an idealized model of an atrial trabeculum. Excitable membrane characteristics of the atrial cell are specified in terms of a Hodgkin-Huxley type of model that is quantitatively based on single-microelectrode voltage clamp data from bullfrog atrial myocytes. This membrane model can simulate the behavior of normal cells as well as of ischemic cells that exhibit depressed electrophysiological behavior (e.g., decreased resting potential, upstroke velocity, peak height, and action potential duration). Depressed activity can be easily simulated with variation of a single model parameter, the gain of the Na+/K+ pump current (INaK). Intercellular coupling properties are specified in terms of a lumped resistive T-type network between adjacent cells. The atrial strand model provides a means for studying the theoretical aspects of slow conduction in a "hybrid" strand that consists of a central region of cells having abnormal membrane or coupling properties, flanked on either side by normal atrial cells. Both uniform and discontinuous conduction are simulated by means of appropriate changes in the coupling resistance between cells. In addition, by varying either the degree of depressed electrical activity or the intercalated disc resistance in the central zone of the strand, slow conduction or complete conduction block in that region is demonstrated. Since the cellular model used in this study is based on experimental data and closely mimics both the atrial action potential and the underlying membrane currents, it has the potential to (1) accurately represent the current and voltage wave-forms occurring in the region of intercalated discs and (2) provide detailed information regarding the mechanisms in intercellular current spread in the region of slow conduction.
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PMID:A model of slow conduction in bullfrog atrial trabeculae. 180 76

Excitable nerve membranes and models for their electrical activity exhibit a broad repertoire of dynamic behavior. To reveal these behaviors the theoretician seeks a model that is simple enough to analyze yet one that retains adequate biophysical realism. Here we strike such a balance by describing a two-variable simplification of the Hodgkin-Huxley (HH) model, which exhibits many membrane phenomena and reproduces, with good agreement, many HH responses. Comparisons and illustrations are presented for the single spike response, repetitive firing (and its cessation by a brief current pulse), and bistable behavior for increased extracellular K+ concentrations.
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PMID:Excitation dynamics: insights from simplified membrane models. 241 1

1. A compartmental model was employed to investigate the electrical behavior of a dendritic spine having excitable membrane at the spine head. Here we used the Hodgkin and Huxley equations to generate excitable membrane properties; in some cases the kinetics were modified to get a longer duration action potential. Passive membrane was assumed for both the spine stem and the dendritic shaft. Synaptic input was modeled as a transient conductance increase (alpha-function) that lies in series with a battery (that corresponds to an excitatory or inhibitory synaptic equilibrium potential). 2. Threshold conditions for an action potential at the spine head membrane were found to be sensitive to the membrane properties at the spine head and to the conductance loading provided by the spine stem and the dendritic tree. Increasing either the number or the open times of the excitable channels had the effect of lowering spike threshold voltage. Increasing the spine stem resistance (RSS) or increasing the input resistance at the spinal base (RSB) also lowered the spike threshold voltage. Because a preexisting dendritic depolarization reduced the spine stem current, this lowered the spike threshold voltage, and this threshold was also shown to be sensitive to the distribution of membrane potential along the dendrite. 3. For each set of spine and dendritic parameters, there was an optimal range of RSS values for which the excitable properties at the spine head membrane resulted in maximal amplification of the dendritic excitatory postsynaptic potential (EPSP), when compared with that produced by a corresponding passive spine. This optimal range depended (with nonlinear sensitivity) on the properties of the voltage-gated channels at the spine head membrane. The maximal amplification found (for each of several sets of parameters) ranged from two to thirteen times. 4. Near this optimal range of RSS values, there was maximal (nonlinear) sensitivity of the dendritic EPSP amplitude to small changes in RSS. A minor decrease resulted in a subthreshold response at the spine head, and this resulted in a large decrease in the EPSP amplitude at the spine base. Increasing the value of RSS above this optimal range decreased the amount of spine stem current flowing to the spine base (by Ohm's law); this decreased the EPSP amplitude at the spine base. The demonstration of this optimum agrees with earlier expectations and results. 5. Excitable dendritic spines can be seen to provide an anatomical arrangement that economizes both excitable and synaptic channels. A small number of these channels (located in spine head membrane) can produce a large dendritic depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Computational study of an excitable dendritic spine. 245 20

Excitable systems can have more than one response threshold, but accessing each of these is only facilitated by preferential choice of the appropriate components in the input noise. The coherence resonance phenomenon discovered by Pikovsky and Kurths [Phys. Rev. Lett. 78, 775 (1997)] utilizes only one response threshold, thus leaving the nature of the dynamics of a possible second threshold unspecified. Here we show using a FitzHugh-Nagumo excitable system that the second response threshold can be reached transiently by brief pulses in the negative noise component, leading to a coherence resonance phenomenon of its own. The resonance can occur both as a function of input amplitude and frequency. The phenomenon is also illustrated in more realistic Hodgkin-Huxley model equations, and analytical predictions are made using probabilistic considerations of the input. This phenomenon attributes more complex role noise can play in excitable systems.
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PMID:Coherence resonance due to transient thresholds in excitable systems. 2086 73

Excitable cells and cell membranes are often modeled by the simple yet elegant parallel resistor-capacitor circuit. However, studies have shown that the passive properties of membranes may be more appropriately modeled with a non-ideal capacitor, in which the current-voltage relationship is given by a fractional-order derivative. Fractional-order membrane potential dynamics introduce capacitive memory effects, i.e., dynamics are influenced by a weighted sum of the membrane potential prior history. However, it is not clear to what extent fractional-order dynamics may alter the properties of active excitable cells. In this study, we investigate the spiking properties of the neuronal membrane patch, nerve axon, and neural networks described by the fractional-order Hodgkin-Huxley neuron model. We find that in the membrane patch model, as fractional-order decreases, i.e., a greater influence of membrane potential memory, peak sodium and potassium currents are altered, and spike frequency and amplitude are generally reduced. In the nerve axon, the velocity of spike propagation increases as fractional-order decreases, while in a neural network, electrical activity is more likely to cease for smaller fractional-order. Importantly, we demonstrate that the modulation of the peak ionic currents that occurs for reduced fractional-order alone fails to reproduce many of the key alterations in spiking properties, suggesting that membrane capacitive memory and fractional-order membrane potential dynamics are important and necessary to reproduce neuronal electrical activity.
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PMID:Membrane capacitive memory alters spiking in neurons described by the fractional-order Hodgkin-Huxley model. 2597 May 34

Excitable lasers with saturable absorbers are currently investigated as potential candidates for low level spike processing tasks in integrated optical platforms. Following a small perturbation of a stable equilibrium, a single and intense laser pulse can be generated before returning to rest. Motivated by recent experiments [Selmi et al., Phys. Rev. E 94, 042219 (2016)10.1103/PhysRevE.94.042219], we consider the rate equations for a laser containing a saturable absorber (LSA) and analyze the effects of different initial perturbations. With its three steady states and following Hodgkin classification, the LSA is a Type I excitable system. By contrast to perturbations on the intensity leading to the same intensity pulse, perturbations on the gain generate pulses of different amplitudes. We explain these distinct behaviors by analyzing the slow-fast dynamics of the laser in each case. We first consider a two-variable LSA model for which the conditions of excitability can be explored in the phase plane in a transparent manner. We then concentrate on the full three variable LSA equations and analyze its solutions near a degenerate steady bifurcation point. This analysis generalizes previous results [Dubbeldam et al., Phys. Rev. E 60, 6580 (1999)1063-651X10.1103/PhysRevE.60.6580] for unequal carrier density rates. Last, we discuss a fundamental difference between neuron and laser models.
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PMID:Two distinct excitable responses for a laser with a saturable absorber. 3001 74