Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Sodium currents after repolarization to more negative potentials after initial activation were digitally recorded in voltage-clamped Myxicola axons compensated for series resistance. The results are inconsistent with a Hodgkin-Huxley-type kinetic scheme. At potentials more negative than -50 mV, the Na+ tails show two distinct time constants, while at more positive potentials only a single exponential process can be resolved. The time-course of the tail currents was totally unaffected when tetrodotoxin (TTX) was added to reduce gNa to low values, demonstrating the absence of any artifact dependent on membrane current. Tail currents were altered by [Ca++] in a manner consistent with a simple alteration in surface potential. Asymmetry current "off" responses are well described by a single exponential. The time constant for this response averaged 2.3 times larger than that for the rapid component of the Na+ repolarization current and was not sensitive to pulse amplitude or duration, although it did vary with holding potential. Other asymmetry current observations confirm previous reports on Myxicola.
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PMID:Characteristics of sodium tail currents in Myxicola axons. Comparison with membrane asymmetry currents. 88 Mar 22

1. Sodium currents (INa) and asymmetrical displacement currents (ID) were measured in the same nerve fibres from Rana esculenta under similar conditions. 2. For exploring possible kinetic and steady state relations between INa and ID the following quantities were compared: (i) the activation of the sodium channels and (ii) the charge displacement of ID. 3. The delay of sodium activation increased after hyperpolarization. A corresponding effect on the displacement of charge was not observed. 4. Upon a small depolarization sodium activation rose slower than the displacement of charge, whereas at large depolarizations sodium activation reached a steady level before the charge displacement. 5. Upon repolarization to various levels between -52 and 12 mV relative to the resting potential, the ratio between the time constants of charge displacement and of sodium tail current varied between 3 and 1. 6. In the steady state the sodium activation was one half at about the same potential as the charge displacement but exhibited a clearly steeper voltage dependence. 7. Blocage of sodium channels with tetrodotoxin did not affect the asymmetrical displacement current. Replacing a part of external Na by tris did not alter the sodijm activation process. 8. The results indicate that the asymmetrical displacement of charge may reflect states of the gating mechanism in sodium channels but cannot be considered as a correlate of the Hodgkin Huxley m variable.
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PMID:Asymmetrical displacement current and its relation with the activation of sodium current in the membrane of frog myelinated nerve. 108 37

A characterization of the properties of voltage-gated sodium channels expressed in the human cerebellar medulloblastoma cell line TE671 is presented. Membrane currents were recorded under voltage clamp conditions using the patch clamp technique in both the whole-cell and the excised-patch configurations. Macroscopic sodium currents display a typical transient time course with a sigmoidal rise to a peak followed by an exponential decay. The rates of early activation and subsequent inactivation accelerate and approach a maximum in response to test potentials, V, of greater depolarization. The magnitude of peak sodium current increased from negligible values below V = -50 mV and reached a maximum at V = -3.6 mV +/- 2.7 mV (mean +/- S.E.M., n = 12). Sodium currents reversed at V = + 70 mV, near the predicted Nernst equilibrium potential for a Na+ selective channel. The peak sodium conductance, gpeak increased with depolarizing voltages to a maximum at V = approximately 0 mV, exhibiting half-activation voltage at V approximately equal to -36.8 mV and an e-fold change in gpeak/9.5 mV. The Hodgkin-Huxley inactivation parameter h infinity indicates that at V = -73.6 mV half of the sodium currents were inactivated. Single channel current recordings demonstrated the occurrence of discrete events: the latency for first opening was shorter as the depolarizing pulse became more positive. The single-channel current amplitude was ohmic with a slope conductance, gamma = 17.13 pS +/- 0.66 pS. Sodium channel currents were reversibly blocked by tetrodotoxin (TTX).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Voltage-gated sodium channels expressed in the human cerebellar medulloblastoma cell line TE671. 216 39

Sodium currents were studied in granule cells dissociated from rat cerebellum. Macroscopic currents were recorded using the patch-clamp technique. Sodium currents, which are TTX sensitive, reached a maximum peak value of 0.42 +/- 0.08 pA/microns2 at 18.4 +/- 2.2 mV (n = 6). Activation and inactivation kinetics and steady-state properties were described in terms of Hodgkin and Huxley parameters. The properties of sodium channels in cultured rat cerebellar granule cells are very similar to those reported for various neural preparations.
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PMID:Voltage dependent sodium currents in cultured rat cerebellar granule cells. 217 5

Sodium currents, INa, were recorded from Xenopus laevis oocytes which had been injected with mRNA synthesized by in vitro transcription of the rat brain sodium channel II cDNA (Noda et al. 1986 a, b). Patch pipettes were used to apply depolarizing voltage steps and to record macroscopic sodium currents of between 50 and 750 pA from cell-attached patches of the oocyte membrane. With a combination of whole-cell and patch clamp recording, the properties of the implanted sodium channels could be studied in detail. They were analyzed according to the model of Hodgkin and Huxley (1952 a) assuming three activation gates. The activation of the sodium currents is characterized by an equilibrium potential of -29 mV and an apparent gating charge of 8.7 e0. At -64 mV half of the sodium currents were inactivated. From single-channel current recordings, an elementary sodium channel conductance of 19 pS and an average open time of 0.43 ms were obtained at -32 mV membrane potential and 16 degrees C. The single-channel and activation properties of rat brain sodium channel II are therefore comparable to those found in peripheral nerve and skeletal muscle, but inactivation occurs at less negative potentials. This could be a specific property of the brain sodium channels and may underlie the maintained inward sodium currents reported in brain neurones (French and Gage 1985).
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PMID:Patch clamp characterization of sodium channels expressed from rat brain cDNA. 243 40

The experiments were done on voltage-clamped nodes of Ranvier of the frog. The aim was to study the kinetics of sodium current INa and gating current Igat over a large potential range (-92 to -12 mV) and to compare the time constants for the turning-on of INa or Igat with those for the turning-off measured at the same potential. Sodium tail currents were recorded at different postpulse potentials. Inactivation was inhibited by a few min treatment with 0.5 mM chloramine-T (Wang 1984). The sodium permeability was activated by a 0.4 ms pulse from holding potential (-92 mV) to about 0 mV. At the peak of INa the membrane was repolarized to postpulse potentials between -92 and -12 mV. At E greater than -60 mV the tail currents decayed with two time constants, tau 1 and tau 2, reflecting presumably the turning-off and the inactivation of the sodium permeability. The relation between tau 1 and postpulse potential was bellshaped with a maximum at -32 mV. The tail currents could also be fitted by the Hodgkin-Huxley equation with the sodium activation variable m raised to the second or third power. At E less than -50 mV tau m off was equal to 2 tau 1 or 3 tau 1, respectively, whereas at E greater than -25 mV tau m off was equal to tau 1. In addition, the time constant of the turning-on of sodium activation m (tau m on) was determined, assuming INa approximately m2 (with a small initial delay) or INa approximately m3 (without an initial delay). At -22 mV and -12 mV the ratio tau m off/tau m on was close to 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of sodium current and gating current in the frog node of Ranvier. 348 38

Membrane potential and current were studied in cut end fibres of frog skeletal muscle under current and voltage clamp conditions, by the double sucrose gap technique. Similar action potentials were recorded under current clamp conditions with either the microelectrode or the double sucrose gap techniques. Under voltage clamp conditions, the control of the membrane potential was maintained adequately. The early current was sensitive to both TTX and external Na concentration suggesting that the current was carried by Na ions. Sodium current (INa) was subsequently analysed using the Hodgkin-Huxley formulae. INa half-activation and inactivation occurred at -34 mV and -60 mV, respectively. Na-rich solution applied internally by diffusion through cut ends produced a reduction of INa associated with a shift of the sodium current reversal potential (VNa) towards more negative membrane potentials. This suggested that the sodium electromotive force was reduced by the increase in internal Na content of the fibre. Iodate applied externally changed neither the activation nor the inactivation time courses of INa, but reduced the peak current. Conversely, internally applied by diffusion from the cut end of skeletal muscle fibre, iodate slowed down the time course of INa inactivation and decreased the current peak. In conclusion, the double sucrose gap technique adapted to cut end frog skeletal muscle fibre allows a satisfactory analysis of INa.
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PMID:Voltage-clamp of cut-end skeletal muscle fibre: a diffusion experiment. 349 62

Single fibres from the sartorius muscle of the toad Bufo marinus were used to study ionic currents, using a fast voltage-clamp method. Sodium currents were analysed following Hodgkin-Huxley formulations. Internal caesium fluoride blocks delayed currents but produced shifts in the equilibrium potential of the early channel due to sodium accumulation. Delayed channels are very unstable when fluoride is used inside the fibre. These instabilities and equilibrium potential shifts were eliminated on replacing fluoride by aspartate in the internal solution. Late peaks of inward current, probably associated with activity at the tubular system, were occasionally observed for small depolarizations. The results are compared with those obtained for other amphibian species and used to explain more general electrophysiological properties of muscle fibres of this tropical toad.
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PMID:Sodium currents in skeletal muscle fibres from the toad Bufo marinus. 608 56

The effects of methyl butyl ketone, methyl heptyl ketone and methyl pentanoate on the sodium current of the squid giant axon have been examined. The peak inward current in intact axons was reduced reversibly by each substance. Sodium currents were recorded in intracellularly perfused axons before and during exposure to the test substances and the records were fitted with equations similar to those proposed by Hodgkin & Huxley (1952). Shifts in the voltage dependence of the steady-state activation and inactivation parameters (m infinity and h infinity), reductions in the peak heights of the activation and inactivation time constants (tau m and tau h) and changes in the maximum sodium conductance (gNa) caused by these substances have been tabulated and compared with the effects of methyl octanoate (Haydon & Urban, 1983b). Each compound shifted the voltage dependence of the steady-state inactivation parameter in the hyperpolarizing direction and that of the steady-state activation parameter in the depolarizing direction. The shifts produced by the ketones are compared with those produced by methyl pentanoate and by methyl octanoate. The possible role of an interaction between the carbonyl oxygen of the test substance and the sodium channel protein in producing the h infinity shift is discussed. The peak time constants are reduced and the voltage dependences of tau m and tau h are shifted in a direction commensurate with the shifts in steady-state properties. The maximum sodium conductance is not much affected either by the ketones or by methyl pentanoate. Large reductions in peak inward current coupled with little effect on gNa have been reported for the n-alkanols and other surface-active compounds (Haydon & Urban, 1983b). This lack of a large effect on gNa indicates that whatever direct interaction does take place between the test substance and the channel protein, it does not result in a blockage of the channel.
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PMID:Anaesthetic action of esters and ketones: evidence for an interaction with the sodium channel protein in squid axons. 609 Jun 52


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