Sodium Tail Research Articles

Can the Sodium Tail of Comet Hale-Bopp Have a Dust-Impact Origin?

Consideration is given to the possible mechanisms responsible for the production of the atomic sodium tail of comet Hale-Bopp. It is shown that both photosputtering and ion sputtering of nonvolatile dust grains might not be the main driving force. Instead, the generation of impact vapor by collisional interaction between the cometary dust coma of micron-sized particles and the very small grains (VSGs) of 10-100 Å size could possibly account for the observations if a large amount of VSGs existed in the coma region.

Three tails of comet Hale‐Bopp

We report on the imaging detection of the sodium tail of comet Hale‐Bopp using large field‐of‐view, multi‐wavelength observations from the McDonald Observatory in March 1997. We subtract off‐band images from sodium‐filter images to obtain the atomic sodium tail, and we find it to be more extended in width than either the dust or ion tails. The cross‐tail integrated brightness of the sodium tail increases with distance from the nucleus for at least 8 million km. The direction of the sodium tail in our data is different from the ion tail, the dust tail, and the sodium tails imaged at different times by other observers. To account for these characteristics, there must be an extended source of sodium atoms tailward of the comet nucleus. We propose that the sodium tail in March 1997 was produced by the release of sodium atoms from grains in the dust tail.

A defect in skeletal muscle sodium channel deactivation exacerbates hyperexcitability in human paramyotonia congenita.

1. Paramyotonia congenita (PC) is a human hereditary disorder wherein missense mutations in the skeletal muscle sodium channel lead to cold-exacerbated muscle hyperexcitability. The most common site for PC mutations is the outermost arginine of domain i.v. segment 4 (human R1448, rat R1441). 2. We examined the rat homologues of two PC mutants with changes at this site: R1441P and R1441C. The R-->P mutation leads to the most clinically severe form of the disease. Since PC has so far been attributed to defects in fast inactivation, we expected the R-->P substitution to have a more dramatic effect on fast inactivation than R-->C. Both mutants (R1441P and R1441C), however, had identical rates and voltage dependence of fast inactivation and activation. 3. R1441P and R1441C also had slowed deactivation, compared with wild-type, raising the possibility that slowed deactivation, in combination with defective fast inactivation, might be a contributing cause of paramyotonia congenita. Furthermore, deactivation was slower in R1441P than in R1441C, suggesting that the worse phenotype of the human R-->P mutation is due to a greater effect on deactivation, and supporting our hypothesis that slowed sodium channel deactivation contributes to paramyotonia congenita. 4. We show that the downstroke of the muscle action potential produced a sodium tail current, and thus slowed deactivation opposes repolarization and therefore leads to hyperexcitability. Hyperexcitability due to slowed deactivation, which has previously been overlooked, also predicts the temperature sensitivity of PC, which has otherwise not been adequately explained.

The Spatial Distribution of Gaseous Atomic Sodium in the Comae of Comets: Evidence for Direct Nucleus and Extended Plasma Sources

Sodium D-line emission (5890 and 5896 Å) has been observed in bright comets at small to moderate heliocentric distances for many years. We present here the first in depth study of a set of spatial profiles of the sodium D-line emission constructed from long-slit spectroscopic observations of Comets Bennett C/1969 Y1, Kohoutek C/1973 D1, and 1P/Halley. Preliminary analysis of these data lead to the suggestion by Combiet al.(1996,A Plasmagenic Source for Gaseous Sodium in Comets.Presented at Asteroids, Comets, Meteors) that a major fraction of the gaseous sodium was produced by an extended source in the tail and that the source was likely to be some charged species. Dissociative recombination of a molecular ion was suggested. The spatial profiles of sodium are not like typical neutral species. The inner region from the nucleus (<2 × 104km) can be explained in terms of a model that accounts for collisional entrainment in the expanding coma and the heliocentric velocity dependent fluorescence rate and radiation pressure acceleration. This source comes either directly from the nucleus or has a very short-lived parent (⪡103s). Away from the nucleus, down the tail and to the sides, the spatial profile slope flattens, indicating a second extended source. The striking similarity of the extended region of sodium spatial profiles with those of ions (H2O+), both along and perpendicular to the tail, is highly suggestive that an ion source is responsible for the production of the extended component of gaseous sodium in the coma. The production rate of the highly variable extended source when present is four to five times that of the direct nucleus source. Observations (Schneideret al., 1991,Science253,1394–1397) and quantitative model analyses (Wilson and Schneider, 1994,Icarus111,31–34) have shown that a dissociative recombination of a sodium bearing molecular ion (NaX+) produces a peculiar component of the neutral sodium near Io. It displays a variable spatial morphology consistent with that of a molecular ion source “picked-up” in the plasma torus corotating with Jupiter's magnetic field. The rapid onset of the appearance of gaseous sodium in bright comets, its spatial distribution in the extended coma and near tail, and recent observations of sodium tails are all consistent with our original suggestion of this plasma source for sodium in comets.

The L1014F Point Mutation in the House Fly Vssc1 Sodium Channel Confers Knockdown Resistance to Pyrethroids

Voltage-sensitive sodium channels encoded by a full-length cDNA corresponding to the Vssc1 gene of the house fly ( Musca domestica) were expressed in Xenopus laevis oocytes either alone or in combination with the tipE gene product of Drosophila melanogaster and were characterized by two-electrode voltage clamp. Vssc1 cRNA alone produced very small (50–150 nA) sodium currents, whereas the combination of Vssc1 and tipE cRNAs produced robust (0.5–3 μA), rapidly inactivating sodium currents. The pyrethroid insecticide cismethrin prolonged the sodium current carried by Vssc1/tipE sodium channels during a depolarizing pulse and induced a tail current after repolarization. The Vssc1 cDNA was specifically mutated to substitute phenylalanine for leucine at position 1014 of the inferred amino acid sequence (L1014F), a polymorphism shown previously to be associated with the kdr (knockdown resistance) trait of the house fly. The L1014F substitution reduced the sensitivity of expressed house fly sodium channels to cismethrin at least 10-fold and increased the rate of decay of pyrethroid-induced sodium tail currents. These results demonstrate that the resistance-associated L1014F mutation confers a reduction in the sensitivity of house fly sodium channels to pyrethroids that is sufficient to account for the kdr resistance trait.

High‐sodium comet

In mid‐April, astronomers in the Canary Islands discovered that Comet Hale‐Bopp has a tail composed of sodium atoms, in addition to the commonly known ion and dust tails. Although sodium atoms have been seen at the centers of other comets, this is the first observation of a comet tail consisting of sodium.The discovery by Gabriele Cremonese of the Padova Astronomical Observatory in Italy and Don Pollaco of the Isaac Newton Group of telescopes at the Canary Islands, came from images of Hale‐Bopp taken with a special wide‐field camera fitted with a filter that isolates emission from sodium atoms. The sodium atoms are distributed over an enormous region in and around Hale‐Bopp. It is not clear exactly how the sodium tail, which is 600,000 km wide and 50 million km long, was formed.

Sodium In Comets

A great deal of attention has been given to the production and spatial distribution of sodium in comets after the discovery of the sodium tail, by Cremonese et al. (1997a), on Hale-Bopp. The sodium has been observed in several comets in the past, but the Hale-Bopp represent the first time where it will be deeply analyzed considering the several data and scientists working on that. The sodium tail stimulated different studies trying to explain the mechanism source and provided the new lifetime for photoionization of the neutral sodium atom. We took into account other sodium observations performed in this century and we focalized our attention to comet Hale-Bopp to understand the main sources responsible for the sodium features observed. We analyzed the sodium tail observations performed by Cremonese et al. (1997b) and Wilson et al. (1998) finding that the Hale-Bopp had four different tails. The wide field images and the high resolution spectroscopy performed along the sodium tail provided very important clues to distinguish the two sodium tails observed and their possible sources. Considering most of the data reported in several papers has been possible to draw a real sketch on what has occurred to the comet during March and April 1997. We are going to demonstrate that the sodium tail observed by Wilson et al. (1998) was not the same reportedby Cremonese et al. (1997a) and in the images taken by the European Hale-Bopp Team there were two distinct sodium tails. The observations allowed us to define “narrow sodium tail” the tail reported by Cremonese et al. (1997a), and “diffuse sodium tail” the tail overimposed to the dust tail. We suggest that the narrow sodium tail was due to a molecular process instead of the diffuse one due to the release of sodium atoms by the dust particles. Such a conclusion is supported by the spatial distribution of sodium on the nucleus and in the coma as reported from other authors.

Quantitative structure-activity studies of pyrethroids: 23. Rate of decrease in sodium tail currents induced by substituted benzyl chrysanthemates and pyrethrates in crayfish giant axons

The effects of pyrethroids, meta-substituted benzyl esters of (1 R)- trans-chrysanthemic and (1 R)- trans-( E)-pyrethric acids, on sodium currents were examined with crayfish giant axons perfused internally. The sodium currents were measured with step depolarization under voltage clamp conditions by the sucrose gap method. The compounds decreased the rate of fall in the tail current that was observed upon step repolarization of the membrane. Variations in the potency to decrease the rate of fall (the tail-current potency) were quantitatively analyzed by use of physicochemical and structural parameters of the aromatic substituents and regression analysis. Structural effects were common to both series of compounds. The introduction of substituents with a phenyl group into the benzyl benzene ring was favorable for the activity. The tail-current potency was also governed by steric dimensions of the substituents in terms of STERIMOL parameters. The aromatic substituents had an optimum width for the potency. The shorter the substituents, the higher was the tail-current potency. Variations in the insecticidal potency of chrysanthemates and pyrethrates against American cockroaches were related linearly with the tail-current potency when the transport factors of compounds were separated by use of the hydrophobicity parameter. The higher the tail-current potency, the higher the insecticidal potency.

Quantitative structure-activity studies of pyrethroids: 16. Physicochemical and structural effects of tetramethrin and related compounds on the decay of sodium tail currents in crayfish giant axons

Effects of tetramethrin and related compounds that have a lactam or an imide structure in the alcohol moiety on sodium currents in internally perfused giant axons of crayfish were examined. The sodium currents were measured with a step depolarizing pulse under voltage clamp conditions using the double sucrose gap method. The compounds decreased the rate of fall of the tail current that was induced upon the step repolarization from the depolarizing phase of the axonal membrane. Variations in the activity to decrease the rate of fall were quantitatively analyzed with reference to the physicochemical parameters of the compounds. The activity of compounds with the lactam structure in the alcohol moiety was lower than that with the imide structure, other things being equivalent. Representing and separating this structural factor with an indicator variable, variations in the activity of the compounds were parabolically related to the steric bulkiness of their alcohol moiety. The whole-body symptomatic activities of the compounds against American cockroaches and their extracellularly measured neurophysiological activities on the cockroach nerve cords were correlated to the activity to decrease the rate of fall of the tail current when transport factors of compounds were considered using the hydrophobicity parameter.

Temperature-dependent subconducting states and kinetics of deltamethrin-modified sodium channels of neuroblastoma cells

The effects of temperature on the properties of sodium channels from mouse neuroblastoma cells modified by the pyrethroid insecticide deltamethrin were investigated using the patch-clamp technique. The study was aimed at determining various states of modified channels which were expected to be revealed by raising the temperature as a result of an increase in channel activity. After exposure to 10 microM deltamethrin, the decay of whole cell sodium current at -30 mV was drastically slowed. It is expressed by two exponential functions at 11 degrees C and by three exponential functions at room temperature (22 +/- 1 degree C). Thus, raising the temperature reveals a new process. Whole cell sodium tail currents associated with step repolarization from -30 mV to -100 mV were best fit by the sum of two exponential functions both at 11 degrees C and at room temperature. The decay of the summed modified single sodium channel currents at -30 mV was expressed by a single exponential function at 11 degrees C, and by two exponential functions at room temperature. In keeping with these results, the open time histograms show the single (11 degrees C) and double (room temperature) exponential distributions. Thus, raising the temperature allows a new single channel process to be revealed. Other modified open states observed previously at 11 degrees C were also found at room temperature including a flickering state and a subconducting state. In addition, several new subconducting states were found at room temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

The action of pyrethroids on sodium channels in myelinated nerve fibres and spinal ganglion cells of the frog

The interaction of pyrethroids with the voltage-dependent sodium channel was studied in voltage-clamped nodes of Ranvier and isolated spinal ganglion neurons of the clawed frog, Xenopus laevis. In the node, pyrethroids prolonged the sodium tail current associated with a step repolarization of the membrane. It was found that the amplitude of the slow, pyrethroid-induced, sodium tail current (PIT) first increased and then decreased as a function of the duration of membrane depolarization (to −5 mV). This decrease of the PIT amplitude was absent when depolarizations to the sodium equilibrium potential (+40 mV) were used. Measurements of changes in sodium reversal potential indicated that sodium ion depletion in the perinodal space is largely responsible for the inactivation of the pyrethroid-modified sodium current. Inactivation is not completely abolished by pyrethroid treatment since the probability of channel opening, measured in membrane patches excised from spinal ganglion cells, decreased slowly during prolonged depolarization. Analysis of unitary currents indicated that both activation and inactivation are retarded by pyrethroids. The arrival of sodium channels in the pyrethroid-modified open state followed a time course that was slower than both activation and inactivation of unmodified sodium channels. Our findings indicate that sodium channels are modified when in the closed resting state and that both opening and closing kinetics are delayed by pyrethroids.

Two open states or two different Na channels in skeletal muscle fibers: Markov models of the decay of Na currents in frog skeletal muscle

The rate of sodium current decay at −140 mV was studied as a function of the duration and amplitude of the activating voltage pulse. These sodium current decays or tails of current showed a biexponential decline in amplitude which depended upon the duration of the activating pulse. At 12°C, the two exponential components of the Na tail currents exhibited time constants of 72 and 534 μs. As the duration of an activating pulse was lengthened, the relative amplitude of the slow component of the decay increased compared to the fast component, without any changes in the fast and slow time constants. This slowing of the decay of current as a function of the duration of the activating pulse is found only in fibers with inactivation intact. A number of Markov models were tested for their ability to predict the biexponential decays found in muscle fibers with inactivation intact and removed. A homogeneous population of channels having only a single open state fails to predict the behavior. A homogeneous population of channels having two open states predicts the behavior. The behavior can also be predicted by two different types of single open-state sodium channels, with one ensemble of channels carrying a minority of the current and exhibiting a much slower closing rate. If a homogeneous population of channels is present, the simulations show that the observed changes in decay rates are driven by inactivation.

Chemical modification of sodium channel inactivation: separate sites for the action of grayanotoxin and tetramethrin

The gating mechanisms of the sodium channel are known to be modified by grayanotoxin and the pyrethroid tetramethrin. Voltage clamp experiments with internally perfused squid giant axons were performed to determine whether or not these two chemicals shared a common site of action in exerting their effects. An additive effect of the two drugs in prolonging sodium currents was observed. Additionally, the characteristics tetramethrin-induced sodium tail current and the grayanotoxin-induced hyperpolarizing shift in the voltage that activated the sodium current were observed simultaneously and independently of the order of drug introduction. Inactive stereoisomers of tetramethrin, which are known to prevent the active tetramethrin stereoisomers from exerting their effect, had no effect on the development of the grayanotoxin-induced modifications of sodium current. It was concluded that tetramethrin and grayanotoxin act at separate sites of action in modifying the sodium channel gating mechanisms in the squid axon membrane.

Interactions of pyrethroids and octylguanidine with sodium channels of squid giant axons

Kinetics of pyrethroid-modified sodium channels and the interaction of N-octylguanidine with the modified channels have been studied with internally perfused and voltage-clamped squid giant axons. The pyrethroids used were 1R- cis-phenothrin; IR- cis-permethrin; 1R- cis-cyphenothrin; and 1R- cis-deltamethrin. Modification of sodium channels by pyrethroids resulted in marked slowing of opening and closing kinetics. The rate at which sodium channels arrived at the open pyrethroid-modified state during a depolarizing step was independent of the concentration of pyrethroids applied. The time of exposure to pyrethroids required for the pyrethroid-induced sodium tail current following a step depolarization to reach a steady-state amplitude was independent of the frequency of short (5ms) depolarizing pulses, and in the pronase-treated axons was independent of the membrane potential (0 mV or– 90 mV). We conclude that sodium channels are modified by pyrethroids primarily in the closed resting state. A small fraction of sodium channels is modified in the open state. The dose-response curve for N-octylguanidine block of sodium channels was not shifted by pyrethroids. The rate at which the pyrethroid-modified sodium channels were blocked by octylguanidine during a depolarizing step depended neither on the concentration of pyrethroids nor on the depolarizing potential, but depended on the concentration of octylguanidine. The time course of the pyrethroid-induced slow sodium tail current was not altered by octylguanidine. We conclude that the actions of pyrethroids and N-octylguanidine on sodium channels are independent of each other.

Increase of sodium current after pyrethroid insecticides in mouse neuroblastoma cells

The effects of 4 different pyrethroid insecticides on sodium channel gating in internally perfused, cultured mouse neuroblastoma cells (N1E-115) were studied using the suction pipette, voltage clamp technique. Pyrethroids increased the amplitude of the sodium current, sometimes by more than 200%. Activation of the sodium current occurred at more hyperpolarized potentials than under control conditions. The declining phase of the sodium current during depolarization was markedly slowed down and after repolarization of the membrane a large, slowly decaying sodium tail current developed. Pyrethroids did not affect the sodium current reversal potential, steady-state sodium inactivation or recovery from sodium channel inactivation. The amplitude of the pyrethroid-induced slow tail current was always proportional to the sodium current at the end of the preceding depolarizing pulse. The rate of decay of the slow tail current strongly depended on pyrethroid structure and increased in the order deltamethrin, cyphenothrin, fenfluthrin and phenothrin. The rate of decay further depended on membrane potential and temperature. Below −85 mV the instantaneous current-voltage relationship of the slow tail current showed a negative slope conductance. The tail current decayed more slowly at low temperatures. Arrhenius plots indicated that the relaxation of open sodium channels to a closed state involved a higher energy barrier for pyrethroid-affected than for normal channels. The energy barrier was higher after deltamethrin than after the non-cyano pyrethroid fenfluthrin. It is concluded that in mammalian neuronal membrane pyrethroids selectively reduce the rate of closing of sodium channels both during depolarization and after repolarization of the nerve membrane.

Supercharging: a method for improving patch-clamp performance

Patch-clamp performance can be improved without altering the normal headstage configuration described by (Hamill, O. P., A. Marty, E. Neher, B. Sakmann, and F. J. Sigworth, 1981, Pfluegers Arch. Eur. J. Physiol., 391:85-100). The "supercharging" method permits resolution of such fast events as calcium and sodium tail currents. Digital computer modeling and analog electronic simulation were used to identify appropriate shapes for the command voltage and the voltage applied to a capacitor tied to the input of the headstage. The voltage command pulse consists of a step with a brief (5-15 microseconds) rectangular spike on its leading edge. Spike amplitude is a function of the membrane capacitance and the access resistance. The spike drives current through the access resistance and speeds charging of the membrane capacitance, making it possible to complete a voltage step within 5-15 microseconds. Clamping speed is independent of the electrode and feedback resistance over a wide range. The second function of the patch clamp amplifier is current measurement, and good time resolution requires suppression of the capacity transient. This can be accomplished by applying an appropriately shaped voltage to the small capacitor tied to the input of the headstage. Series resistance compensation for ionic current transients does not interfere with supercharging. Although the focus of this paper is on whole cell recording, the supercharging concept may prove useful for single channel and bilayer recording techniques.

Activity of tralomethrin to modify the nerve membrane sodium channel

Deltamethrin is a potent type II pyrethroid insecticide which can modify sodium channel gating kinetics in nerve membranes. The actions of another type II pyrethroid tralomethrin to modify sodium channel kinetics have been ascribed to deltamethrin, to which tralomethrin is known to be converted under certain experimental conditions. The objective of this study was to determine if tralomethrin was intrinsically active in modifying the nerve membrane sodium channel, the major target site of pyrethroids. Experiments were performed using the squid giant axon under voltage-clamp conditions. In axons treated with either pyrethroid, a large sodium tail current was generated upon repolarization from a depolarized level and decayed slowly with a dual exponential time cuurse. The fast time constant for tralomethrin was 165 ± 110 msec and the slow time constant was 3793 ± 802 msec. For deltamethrin the time constants were significantly shorter, the fast time constant being 34 ± 6 msec and the slow time constant being 835 ± 282 msec. The cumulative dose-response relation of tralomethrin revealed two binding sites with apparent dissociation constants of 0.06 and 5 μ m. Deltamethrin appeared to bind to only one site with an apparent dissociation constant of 0.25 μ m. It is clear that there are large differences in the gating kinetics of the sodium channels modified by tralomethrin and deltamethrin which are incompatible with the idea that tralomethrin is active only after conversion to deltamethrin. The differences in sodium channel gating kinetics after modification by tralomethrin versus deltamethrin indicate that tralomethrin is intrinsically active in modifying the nerve membrane sodium channels.

Toxins That Modulate the Sodium Channel Gating Mechanisma

A variety of toxins and chemicals has been shown to modulate the gating kinetics of the sodium channel. Studies of batrachotoxin, grayanotoxins and pyrethroids are summarized here as examples. Batrachotoxin and grayanotoxins eliminate the sodium channel inactivation thereby causing a prolonged, steady-state sodium current to flow during a depolarizing step. The sodium channel activation kinetics are not affected markedly. Batrachotoxin appears to bind to a site in the sodium channel to which the inactivation gate normally binds, thus causing an inhibition of sodium inactivation. Single channel recording experiments have shown that the mean open time of individual sodium channels is greatly prolonged by batrachotoxin. It appears that individual sodium channels are modified by batrachotoxin in an all-or-none manner. Pyrethroids which are synthetic derivatives of pyrethrins also modify the kinetics of sodium channels in a very drastic manner. In the presence of type I pyrethroids which lack a cyano group at the alpha position (e.g., allethrin and tetramethrin), a large steady-state sodium current appears during a step depolarization and a large slowly decaying sodium tail current appears upon repolarization. Thus both the activation and inactivation kinetics are slowed. Type II pyrethroids which contain an alpha-cyano group (e.g., deltamethrin, cyphenothrin, and fenvalerate) exert effects on sodium channels qualitatively similar to those of type I pyrethroids. However, the amplitudes of the steady-state sodium current and sodium tail current are smaller and the time constant of tail current decay is much longer. The mean open time of single sodium channels is greatly prolonged by the pyrethroids, and the effect is much more pronounced in type II than in type I pyrethroids. A high degree of stereospecificity has been found among four isomers of tetramethrin, (+)-trans and (+)-cis isomers being highly active and (-)-trans and (-)-cis isomers almost totally inactive. The inactive isomers bind to the sodium channel sites, thus preventing the action of the active isomers. Because of the unique action of pyrethroids in modulating the sodium channels, they are becoming useful tools for channel physiology and pharmacology.

Kinetics of sodium current and gating current in the frog node of Ranvier.

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)

Ion permeation and selectivity of squid axon sodium channels modified by tetramethrin

The pyrethroid tetramethrin greatly prolongs the sodium current during step depolarization and the sodium tail current associated with step repolarization of the squid axon membrane. Non-linear current-voltage relationships for the sodium tail current were analyzed to assess the open sodium channel properties which included the permeation of various cations, calcium block and cation selectivity. Tetramethrin had no effect on any of these properties. It was concluded that tetramethrin modifies the sodium channel gating machinery without affecting the pore properties.