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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 form of power spectra of K+ conduction fluctuations in patches of squid axon suggested that K+ conduction kinetics are higher than first order (Fishman, Moore & Poussart, 1975, J. Membrane Biol. 24:305). To obtain an alternative description of ion conduction kinetics consistent with spontaneous fluctuations, the complex impedance and admittance of squid (Loligo pealei) axon were measured at low frequencies (1-1000 Hz) with a four electrode system using white Gaussian noise as a stochastic perturbation. As predicted from the spontaneous noise measurements, a low frequency impedance feature is observed between 1 and 30 Hz which is voltage and temperature dependent, disappears after substantial reduction in [Ki+], and is unaffected by the state of Na+ conduction or active transport. These measurements confirm and constitute strong support for the patch noise measurements and interpretations. The linearized Hodgkin-Huxley (HH) equations do not produce the low frequency feature since first order ion conduction kinetics are assumed. Computation of diffusion polarization effects associated with the axon sheath gives a qualitative account of the low frequency feature, but the potential dependence is opposite to that of the data. Thus, K+ conduction kinetics in the axon are not adequately described by a single first order process. In addition, significant changes in HH parameter values were required to describe the usual impedance (resonance) feature in Loligo pealei axon data.
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PMID:K+ conduction description from the low frequency impedance and admittance of squid axon. 86 80

To describe the kinetics of potassium permeability (conductance) changes in the squid giant axon membrane the Hodgkin--Huxley formulation uses a single first-order in time variable n with forward and backward rate constants, respectively alpha-n and beta-n, potential-dependent but time-independent. It has been shown by Frankenhaeuser that in the potassium-carrying system of the myelinated nerve fiber membrane of Xenopus laevis the rate constant beta-n is dependent on the duration of previous depolarization, i. e. the beta-n of this membrane is time-dependent. Started from the FitzHugh--Cole--Moore translation principle for potassium current experimental data of Frankenhaeuser have been analysed to show that the rate constant alpha-n in the X. laevis nerve fiber membrane is also time-dependent. To keep the conventional Hodgkin--Huxley formulation valid in case of the potassium-carrying system of the X. laevis nodal membrane involvement of an additional first--order in time component (n-II) has been postulated, which is compatible with Frankenhaeuser's experimental results. This component n-II appears to be identical to the n-II-component in the potassium-carrying system of the Rana ridibunda nerve fiber membrane. Both are rather slow and activated within the potential range more negative than the basic n-I-component (corresponding to Frankenhaeuser's variable n). The component n-I seems to be identical to the n-component of many other excitable membranes with fast action potentials. The existence of the third, very slow nIII-component is also possible. The independent components in question are believed to be associated with different independent potassium channels within the same membrane. It is likely that the existence of several independent components is a general feature of the potassium-carrying mechanism in the excitable membranes essential for a particular type of electrogenesis.
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PMID:[Time dependence of the reaction rate constant of potassium permeability of Ranvier's node membrane]. 111 3

Activation of potassium conductance in squid axons with membrane depolarization is delayed by conditioning hyperpolarization of the membrane potential. The delayed kinetics superpose with the control kinetics almost, but not quite, exactly following time translation, as demonstrated previously in perfused axons by Clay and Shlesinger (1982). Similar results were obtained in this study from nonperfused axons. The lack of complete superposition argues against the Hodgkin and Huxley (1952) model of potassium conductance. The addition of a single kinetic state to their model, accessible only by membrane hyperpolarization, is sufficient to describe this effect (Young and Moore, 1981).
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PMID:Conditioning hyperpolarization delays in squid axon potassium channels. 242 15

A homomorphism on a physical system of the Hodgkin-Huxley equations for ion conductance in nerve is derived. It is pointed out that a homomorphism can correct the Cole-Moore discrepancy in delay of conductance for voltage clamp data with initial hyperpolarization. The voltage dependence of the rate constants can also be removed. Curves are presented to compare the representation of the nerve conductances by the Hodgkin-Huxley equations and the new homomorphism.
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PMID:Homomorphism on a physical system of the Hodgkin-Huxley equations for ion conductance in nerve. 409 52

Two illustrative molecular models, designed to explain the Cole-Moore K(+) hyperpolarization delay, are proposed and analyzed. Both introduce a process supplementary to the usual Hodgkin-Huxley (HH) one for a K(+) channel. In both cases the new process becomes involved as a consequence of the conditioning hyperpolarization of the membrane and would account for the observed delay time in the K(+) current after depolarization to near ENa. The first model uses adsorption or desorption of phospholipid molecules on the surface of the assumed protein K(+) channel or gate. The second model involves the translocation of the charged subunits of the channel in the hyperpolarizing electric field.
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PMID:On the theory of ion transport across the nerve membrane. V. Two models for the Cole-Moore K + hyperpolarization delay. 504 84

We use a tetrahedral model of four interacting protein subunits to represent the K(+) channel or gate in the squid nerve membrane. The kinetic predictions, with varying degrees of cooperativity, are compared with experimental observations, especially those of Hodgkin and Huxley (J. Physiol. 117, 500, 1952) and of Cole and Moore (Biophys. J. 1, 1, 1960). The tentative conclusion reached is that if there is any cooperativity present it must be rather weak. There is no indication here that cooperativity improves the Hodgkin-Huxley assumption of independent "subunits". Other related models will be discussed in Part III. We also find evidence against the suggestion that there is cooperativity between K(+) channels arranged in patches of a two-dimensional lattice.
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PMID:On the theory of ion transport across the nerve membrane. II. Potassium ion kinetics and cooperativity (with x = 4). 528 56

In the preceding paper (Moore & Westerfield, 1983) the effects of changes in membrane properties and non-uniform geometry on impulse propagation and threshold parameters were investigated. In this paper the contributions of these and other parameters to the site of initiation of an impulse were determined by computer simulations using the Hodgkin-Huxley membrane description, the cable equations, and geometry appropriate for a simplified motoneurone with a non-myelinated axon. Antidromic invasion of action potentials into the soma was found to depend upon (a) the ionic channel rate constants (determined by the temperature), (b) the abruptness of the transition from the small-diameter axon to the larger diameter (and increased load) of the soma-dendrite, (c) extensions of active properties into the dendrite, and (d) density of ion channels. The location of the apparent site of initiation of impulses was not necessarily at the site of synaptic input nor the nearest active membrane. Its position depended upon (a) the fraction of the dendritic tree with excitable membrane, and secondarily on (b) the stimulus strength. Even with uniform excitability in the active membrane, the apparent site of initiation could be moved a considerable distance from the soma and the site of stimulation by appropriate choice of the various parameters noted above.
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PMID:On the site of impulse initiation in a neurone. 630 24

We examined the activation kinetics of the delayed rectifier K+ current of bullfrog sympathetic neurons, primarily using whole cell recording. On depolarization, currents activated with a sigmoid delay but did not show a Cole-Moore shift. The time course of activation differed systematically from an exponential raised to a power. At most voltages, a power of 2 gave the best overall fit but a power of 3 better described the initial delay. After the delay, the time course could be fitted by a single exponential. Time constants were 15-20 ms at 0 mV and decreased to a limiting tau = 7 ms at +50 to +100 mV. Tail currents were well fitted by single exponential functions and accelerated with hyperpolarization, from tau = 15-20 ms at 0 mV to tau = 2 ms at -110 mV (e-fold for 40 mV). Eleven kinetic models were evaluated for their ability to describe the activation kinetics of the delayed rectifier. Hodgkin-Huxley-like models did not fit the data well. A linear model where voltage sensor movement is followed by a distinct channel opening step, allosteric models based on the Monod-Wyman--Changeux model, and an unconstrained C-C-C-O model could describe whole cell data from -100 to +40 mV. After including whole cell data at +60 and +80 mV, and a maximal p(open) of 0.8 from noise analysis of cell-attached patches, an allosteric model fit the data best, as the other models had difficulty describing qualitative features of the data. However, some more complex schemes (with additional free parameters) cannot be excluded. We propose the allosteric model as an empirical description of macroscopic ionic currents, and as a model worth considering in future studies on the molecular mechanism of potassium channel gating.
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PMID:Activation kinetics of the delayed rectifier potassium current of bullfrog sympathetic neurons. 958 10

There are no established conventions for portraying scientific women. At the Royal Society, the first image of a female scientist was Henry Moore's drawing of Dorothy Hodgkin's hands, cruelly twisted by agonising arthritis. In her famous oil portrait, Maggi Hambling also focuses on Hodgkin's hands, thus symbolising the Nobel-prize winner's dedication to research and the importance of manual dexterity. Although Hambling's picture features a model of insulin, it is very different from photographs celebrating the discovery of DNA.
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PMID:Pictures of Dorothy Hodgkin. 1279 14

The voltage clamp results of Hodgkin and Huxley have been reanalyzed in terms of alternative mathematical models. The model used for the potassium conductance changes is similar to that of the HH model except that an empirical functional relationship replaces the fourth power Law used by HH and the twenty-fifth power law used by Cole and Moore. The model used for the sodium conductance changes involves the explicit use of one variable only rather than the two variables m and h of HH. The rise and fall of the sodium conductance during a depolarizing voltage clamp is obtained by specifying that this one variable satisfies a second order differential equation which results from the coupling of two first order equations. Not only can the adjustable parameters of these models be made to give good fit to the clamp conductance data but the models can also then be used to compute action potential curves. Theoretical interpretations can also be given to these mathematical models.
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PMID:THE SQUID GIANT AXON. MATHEMATICAL MODELS. 1406 58


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