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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 theoretical power density spectrum S(f) of ion current noise is calculated from several models of the sodium channel gating mechanism in nerve membrane. Sodium ion noise experimental data from the frog node of Ranvier [Conti, F., et al. (1976), J. Physiol. (London) 262:699] is used as a test of the theoretical results. The motivation for recent modeling has been evidence for a coupling between sodium activation and inactivation from voltage clamp data. The two processes are independent of one another in the Hodgkin and Huxley (HH) model [Hodgkin A.L., Huxley, A.F. (1952), J. Physiol. (London) 117:500]. The noise data is consistent with HH, as noted by Conti et al. (1976). The theoretical results given here appear to indicate that only one case of coupling models is also consistent with the noise data.
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PMID:Comparison of ion current noise predicted from different models of the sodium channel gating mechanism in nerve membrane. 35 12

In experiments on 75 female mice of line SJL/J with lymphograulomatosis, 75 female mice of the same line without lymphogranulomatosis and intact non-lineal mice, the authors have studied the labelled tumorigenic compounds: indium-111, gallium-67-citrates and sodium selenium-75-selenite. It was found that only sodium selenium-75-selenite possesses an enhanced ability to be accumulated in lymphogranulomatosis involved lymph nodes in mice. Whereas indium-111 and gallium-67-citrates contrary to the literature data available showed no enhanced tropism to lymph nodes of mice with lymphogranulomatosis.
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PMID:[Tropism of radiopharmacologic preparations in lymphogramulomatosis in mice]. 46 61

An adsorption model of nerve axon has been extended to account for the origin of membrane currents observed under voltage-clamp conditions. Differing from the Hodgkin-Huxley model, which attributes excitation solely to a change of ionic conductances of the membrane, the present model proposes that a layer of axoplasm attached to the membrane (axon cortex) can undergo conformational changes and hence modulate selectivity for mobile ions. To test the model, a two-step voltage-clamp study was made of the chemical driving forces of Na+ and K+ ions in squid giant axon. The forces were measured by determining the instantaneous current-voltage relation when membrane current is carried by Na+ only or K+ only. The data indicate that the chemical driving force varies as a function of time and does not agree with the Nernst relation during the early phase of excitation. Implications of the observations are discussed.
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PMID:A physical model of nerve axon. II: Action potential and excitation currents. Voltage-clamp studies of chemical driving forces of Na+ and K+ in squid giant axon. 53 Nov 10

A nerve membrane model with a two-state pore system was investigated by computer simulation in the uniform (space-clamped) case. Both sodium and potassium conducting pores were modelled, each pore having four independent gates which switched randomly between the open and the closed position, governed by the assumed rate constants. Each pore conducted only when all the gates were open. The model was based upon the Hodgkin-Huxley equations for the giant axon in squid, and in the limit of an infinite number of pores it was identical to these. The firing behaviour of this model as a function of the number of pores and the injected current were investigated. The mean firing frequency and the distribution of interspike intervals were mainly used in the presentation of the results. It was found that for pore numbers less than about 20 000 the main effects due to a finite number of pores were a lowering of the current threshold for firing and a more linear frequency current relationship relative to that of the original H-H equations. For higher pore numbers an increase in the current threshold and a pronounced burst firing close to the threshold were found.
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PMID:Firing behaviour in a stochastic nerve membrane model based upon the Hodgkin-Huxley equations. 54 28

Calcium current, Ica, was studied in isolated nerve cell bodies of Helix aspersa after suppression of Na+ and K+ currents. The suction pipette method described in the preceding paper was used. Ica rises to a peak value and then subsides exponentially and has a null potential of 150 mV or more and a relationship with [Ca2+]o that is hyperbolic over a small range of [Ca2+]o's. When [Ca2+]i is increased, Ica is reduced disproportionately, but the effect is not hyperbolic. Ica is blocked by extracellular Ni2+, La3+, Cd2+, and Co2+ and is greater when Ba2+ and Sr2+ carry the current. Saturation and blockage are described by a Langmuir adsorption relationship similar to that found in Balanus. Thus, the calcium conductance probably contains a site which binds the ions referred to. The site also appears to be voltage-dependent. Activation and inactivation of Ica are described by first order kinetics, and there is evidence that the processes are coupled. For example, inactivation is delayed slightly in its onset and tau inactivation depends upon the method of study. However, the currents are described equally well by either a noncoupled Hodgkin-Huxley mh scheme or a coupled reaction. Facilitation of Ica by prepulses was not observed. For times up to 50 ms, currents even at small depolarizations were accounted for by suitable adjustment of the activation and inactivation rate constants.
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PMID:The calcium current of Helix neuron. 66 Jan 60

1. Ionic currents in differentiated cells of mouse neuroblastoma clone N1E-115 have been studied under voltage-clamp conditions. 2. Depolarizing voltage steps from a holding potential of -85 mV to levels more positive than -40 mV produced fast transient inward currents followed by delayed outward currents. 3. The fast inward current is carried by Na+: it is blocked by tetrodotoxin and is absent in Na+-free solutions. Its kinetic behaviour resembles that of the Na+ current in squid giant axon. A mean value of 85 mmho/cm2 was found for the maximum Na+ conductance (GNa).4. The delayed outward current is carried primarily by K+: it is blocked by externally applied tetraethylammonium (TEA, 15 mM) and has a reversal potential (mean -71 mV) close to the theoretical K+ equilibrium potential. Its instantaneous I--V curve is linear. By analogy with the formulation of Hodgkin & Huxley (1952c), the outward current can be described by IK = -GKn2(V--EK) where GK = 12 mmho/mc2. 5. During prolonged depolarizations the delayed outward current declines. This decline, which occurs in two phases, represents a partial inactivation of the K+ conductance. 6. A weak inward current with slow activation and inactivation kinetics appears in Na+-free solution containing 10 mM-Ca2+. It is activated at a membrane potential of -55 mV and reaches its maximum at -20 mV with a time to peak of about 10 msec. This current is tetrodotoxin-resistant, reversibly blocked by Co2+ (5mM) and is suggested to be carried by Ca2+. 7. An increase in the external divalent cation concentration results in a parallel shift of the steady-state I--V curve along the voltage axis in positive direction. The activation of delayed outward currents is suggested not to depend on Ca2+ influx. 8. It is concluded that separate voltage-dependent Na+, K+ and Ca2+ channels exist in the differentiated neuroblastoma membrane with kinetic and pharmacological properties similar to those observed in non-mammalian preparations.
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PMID:Ionic currents in cultured mouse neuroblastoma cells under voltage-clamp conditions. 67 Dec 97

The contribution of specific ions to the conductance and potential of the basolateral membrane of the rabbit urinary bladder has been studied with both conventional and ion-specific microelectrode techniques. In addition, the possibility of an electrogenic active transport process located at the basolateral membrane was studied using the polyene antibiotic nystatin. The effect of ion-specific microelectrode impalement damage on intracellular ion activities was examined and a criterion set for acceptance or rejection of intracellular activity measurements. Using this criterion, we found (K+) = 72 mM and (Cl-) = 15.8 mM. Cl- but not K+ was in electrochemical equilibrium across the basolateral membrane. The selective permeability of the basolateral membrane was measured using microelectrodes, and the data analyzed using the Goldman, Hodgkin-Katz equation. The sodium to potassium permeability ratio (PNa/PK) was 0.044, and the chloride to potassium permeability ratio (PCl/PK) was 1.17. Since K+ was not in electrochemical equilibrium, intracellular (K+) is maintained by active metabolic processes, and the basolateral membrane potential is a diffusion potential with K+and C1- the most permeable ions. After depolarizing the basolateral membrane with high serosal potassium bathing solutions and eliminating the apical membrane as a rate limiting step for ion movement using the polyene antibiotic nystatin, we found that the addition of equal aliquots of NaCl to both solutions caused the basolateral membrane potential to hyperpolarize by up to 20mV (cell interior negative). This potential was reduced by 80% within 3 min of the addition of ouabain to the serosal solution. This hyperpolarization most probably represents a ouabain sensitive active transport process sensitive to intracellular Na+. An equivalent electrical circuit for Na+ transport across rabbit urinary bladder is derived, tested, and compared to previous results. This circuit is also used to predict the effects that microelectrode impalement damage will have on individual membrane potentials as well as time-dependent phenomena; e.g., effect of amiloride on apical and basolateral membrane potentials.
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PMID:Basolateral membrane potential of a tight epithelium: ionic diffusion and electrogenic pumps. 67 23

Yohimbine, an indolealkylamine alkaloid, reduces the amplitude of the sodium current in the squid giant axon. For doses that reduce sodium current amplitude by up to 50%, there is no significant change in the kinetics or in any of the voltage-dependent parameters associated with sodium channels. The effective equilibrium constant for yohimbine binding to the sodium channel is 3 x 10(-4) M. Repetitive depolarizing pulses increase the inhibition of squid axon sodium current by yohimbine. This use-dependent inhibition is enhanced by increasing the concentration of yohimbine, by increasing the frequency of pulsing, and by increasing the magnitude or the duration of depolarization. It is reduced by hyperpolarizing prepulses. This behavior can be explained by a model wherein yohimbine binds more readily to open sodium channels than to closed sodium channels and wherein the Hodgkin-Huxley kinetic parameters are modified by the binding of the drug. This type of model may also explain the tonic and use-dependent inhibition previously described by others for local anesthetics.
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PMID:Effects of yohimbine on squid axons. 72 22

The axon membrane is simulated by standard Hodgkin-Huxley leakage and potassium channels plus a coupled transient excited state kinetic scheme for the sodium channel. This scheme for the sodium channel is as proposed previously by the author. Simulations are presented showing the form of the action potential, threshold behavior, accommodation, and repetitive firing. It is seen that the form of the individual action potential, its all-or-none nature, and its refractory period are well simulated by this model, as they are by the standard Hodgkin-Huxley model. However, the model differs markedly from the Hodgkin-Huxley model with respect to repetitive firing and accommodation to stimulating currents of slowly rising intensity, in ways that are shown to be related to those features of the sodium inactivation which are anomalous to the H-H model. The tendency for repetitive firing is highly dependent on that parameter which primarily determines the existence of the inactivation shift in voltage clamp experiments, in such a way that the more pronounced the inactivation shift, the less the tendency for repetitive firing. The tendency for accommodation is highly dependent on that parameter which primarily determines the 'tauc-tauh' separation, in such a way that the greater the separation the greater the tendency for the membrane to accommodate without firing action potentials to a slowly rising current.
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PMID:A fully coupled transient excited state model for the sodium channel. II. Implications for action potential generation, threshold, repetitive firing, and accommodation. 75 Jun 31

Several compounds of fungal or bacterial origin (EIM, alamethicin, monazomycin, DJ400B) can be incorporated into planar lipid bilayers where they form molecular channels and generate voltage-dependent ion conductances. When studied by voltage clamp, the kinetic and steady-state characteristics of these conductance changes are in every respect identical to those found in excitable cell membranes, and their major aspects can be quantitatively described by the Hodgkin-Huxley equations. Thus, the steady-state conductance is an expotential function of the membrane potential, the conductance rises with a sigmoid time course and decays exponentially, and the time constants of the conductance changes go through a maximum as a function of the potential. The conductances also show inactivation as seen in the sodium channels of nerve and the potassium channels of muscle. In addition, there appear for particular pulsing sequences certain kinetic transients that cannot be accounted for by the Hodgkin-Huxley equations but are also seen in identical form in nerve. Because the kinetics are identical in all excitable cell membranes and in these bilayers, it is likely that, in spite of the diverse chemical nature of the channel-forming molecules in the bilayers and the widely differing ion selectivities in the cellular systems, the mechanism by which the membrane opens and closes for the flow of ions is essentially the same in all cases. The kinetic data imply that a cooperative process is involved in the gating action. In principle, two different concepts could account for the kinetics--one involving an intramolecular configurational change within a complex permanent channel, the other, the assembly of a channel through the voltage-dependent aggregation of monomeric channel precursors. In the bilayers the high-order dependence of the steady-state conductance and of the gating time constants on the concentration of the channel formers suggests an aggregation mechanism in which the gating involves the voltage-induced insertion of all or part of the channel-forming molecules from the membrane surface into the hydrocarbon region and their subsequent aggregation into open channels by lateral diffusion. The mathematical description of this two-step insertion-aggregation mechanism accounts quantitatively for the entire conductancb-voltage kinetics including inactivation and other kinetic features which deviate from the Hodgkin-Huxley kinetics in the sense that the rate constants of the changes are dependent not only on the membrane potential but also on the value of the conductance and on time. The proposed mechanism is also in agreement with single-channel data for alamethicin which suggest that both the insertion and the aggregation rate constants are voltage-dependent...
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PMID:Molecular aspects of electrical excitation in lipid bilayers and cell membranes. 77 70


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