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PubMed1981

Effects of internal and external sodium on the sodium current-voltage relationship in the Squid giant axon.

The early transient current-voltage relationship was measured in internally perfused voltage clamped squid giant axons with various concentrations of sodium on the two sides of the membrane. In the absence of sodium on either side there is an outward transient current which is blocked by tetrodotoxin and varies with internal potassium concentration. The current increases linearly with voltage for positive potentials. Adding sodium ions internally increases the slope of the current-voltage relationship. Adding sodium ions externally also increases the slope between +10 and +80 mV. Adding sodium to both sides produces the sum of the two effects. The current-voltage relationships were fit by straight lines between +10 and +80 mV. Plotting the extrapolated intercepts with the current axis against the differences in sodium concentrations gave a straight line, Io = -P (Co-Ci)F. P, the Fickian permeability, is about 10(-4) cm/sec. Plotting the slopes in three dimensions against the two sodium concentrations gave a plane g = go + (aNao + bNai)F. a is about 10(-6) cm/mV-sec and b about 3 x 10(-6) cm/mV-sec. Thus the current-voltage relationship for the sodium current is well described by I = -P(Co-Ci)F+ (aco + bci)FV for positive potentials. This is the linear sum of Fick's Law and Ohm's Law. P/(a + b) = 25 +/- 1 mV (N = 6) and did not vary with the absolute magnitude of the currents. Within experimental error this is equal to kT/e or RT/F. Increasing temperature increased P, a and b proportionately. Adding external calcium, lithium, or Tris selectively decreased P and a without changing b. In the absence of sodium, altering internal and external potassium while observing the early transient currents suggests this channel is more asymmetric in its response to potassium than to sodium.

Animals↗
PubMed1979

Chemically induced K+ conduction noise in squid axon.

Internal perfusion of tetraethylammonium ions (TEA) in squid axons produces a significant high frequency noise component. Although internal TEA suppresses the potassium conductance (GK) noise at relatively low frequencies, it induces high frequency noise which exceeds the intensity of the normal potassium and sodium noise. In addition, the induced noise is dependent on the presence of internal potassium ions (K+) suggesting that this source of noise arises from a modulation of the K+ conductance due to the blocking and unblocking of the K+ channel. The simplest model describing the TEA data is a two-step sequential, pseudo-unimolecular reaction where TEA binds during an open conductance state. A unit channel conductance of 2 pS is estimated from the TEA data as well as noise induced by triethyldecylammonium (TEDA) ions. Thus, these data are consistent with the hypothesis that the channel is blocked whenever the quaternary ammonium ion binding site, located near or within the K+ channel, is occupied.

Animals↗
PubMed1977

Water fluxes in nerve fiber.

The hydrostatic (Lp) and osmotic (LPD) filtration coefficients and the efflux rates of tritiated water were measured in the giant axon of Loligo vulgaris. The Lp was 8 to 14 X 10(-8) cm/sec/cm H2O and the LPD was two orders of magnitude smaller (3 to 6 X 10(-10) cm/sec/cm H2O). In axons whose diameter was approximately 500 micron, the time (t1/2) required for a reduction in the axonal labeled water activity to one half its initial value was 38 to 48 sec. The rate limiting structure for solute flux was made ineffective by (1) storing the axon in isosmotoc KF at 0-2 degrees C for one month to one year or by (2) fixing the axon in 2-4% glutaraldehyde for 3 to 7 hr. The criteria of ineffectiveness of the rate limiting structure for solute flux were (1) a reduction of LPD to immeasurably low values, (2) the absence of electrical properties characteristic of plasmalemma, and (3) a marked increase in the rate of efflux of Na22. In such impaired axons the Lp and the t 1/2 of tritiated water efflux were unaffected. This independence of solute and solvent flux in conjunction with the finding that the hydraulic conductivity determined by bulk osmotic and hydrostatic pressure gradients is not equivalent (i.e., LPD/LP less than 1) indicate that the rate limiting structures for solute and solvent flux are in series. Solvent fluxes appear to be surface-limited, not bulk-limited. We have been unable to resolve whether the surface structure involved in limiting solvent flux is the sheath (Schwann layer and adhering connective tissue) and/or the cortical layer of the axoplasmic gel.

Animals↗
PubMed1977

Osmotic relations of nerve fiber.

The volumetric elastic modulus of the sheath and the osmotic swelling pressure of the axoplasmic polymer network of the giant axon of Loligo vulgaris were measured. Evidence was obtained that (1) the elastic modulus of the sheath, (2) the swelling pressure of axoplasm, and (3) the effective osmotic pressure difference due to mobile solutes determine axonal volume. The contributions of the sheath and the axoplasm were significant because the effective osmotic pressure due to mobile solutes was a small fraction of the theoretical bulk osmotic pressure due to these solutes. The giant axon was converted from an imperfect to a near perfect osmometer by minimizing the contribution of the sheath and the axoplasmic gel.

Animals↗
PubMed1977

K+ conduction description from the low frequency impedance and admittance of squid axon.

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.

Animals↗
PubMed1975

Penetration of phospholipases A2 and C into the squid (Loligo pealii) giant axon.

Following 1 h exposure, the level of phospholipase A2 penetration into the axoplasm of the squid giant axon was 107 to 350% of that in the external media; corresponding values for phospholipase C were 18 to 31%. Phospholipases can therefore be used to study phospholipid function in axons since they can penetrate through connective tissue and Schwann cell to reach the axolemma.

Animals↗
PubMed1984

Axonal microtubules necessary for generation of sodium current in squid giant axons: I. Pharmacological study on sodium current and restoration of sodium current by microtubule proteins and 260K protein.

Effects of the reagents suppressing or supporting axoplasmic microtubule assembly were studied on the Na ionic current of squid giant axons by perfusing the axon internally with the solution containing the reagent. Among the reagents suppressing the assembly, colchicine, vinblastine, podophyllotoxin, sulfhydryl reagents such as DTNB and NEM, and chaotropic anions such as iodide and bromide, were examined. These reagents reduced maximum Na conductance and shifted the voltage dependence of steady-state Na activation in a depolarizing direction along the voltage axis. They also made the voltage dependence less steep, but did not affect sodium inactivation appreciably. Effects on Na ionic current of reagents which support microtubule assembly (Taxol, DMSO, D2O and temperature) were opposite the effects of those agents suppressing assembly. At the same time, we demonstrated that after Na currents were partially reduced, they could be restored by internally perfusing the axon with a solution containing microtubule proteins, 260K proteins and cAMP under conditions favorable for microtubule assembly. For full restoration, it was found that the following conditions were necessary: (1) The microenvironment within the axon is suitable for microtubule assembly. (2) Tubulins incorporated into microtubules are fully tyrosinated at their C-termini. (3) A peripheral protein having a molecular weight of 260,000 daltons (260K protein) is indispensable. These results suggest that axoplasmic microtubules and 260K proteins in the structure underlying the axolemma play a role in generating Na currents in squid giant axons.

Alkaloids↗
PubMed1984

Axonal microtubules necessary for generation of sodium current in squid giant axons: II. Effect of colchicine upon asymmetrical displacement current.

Effect of internal colchicine on asymmetrical displacement currents was studied by internally perfusing squid giant axons with a solution containing colchicine. It was found that (1) asymmetrical displacement currents were composed of two parts; colchicine-sensitive and colchicine-resistant; that (2) the colchicine-sensitive part had a definite rising phase while the colchicine-resistant one showed an instantaneous jump, followed by exponential decay; and that (3) the colchicine-sensitive part related to normal Na channels.

Animals↗
PubMed1978

On the physico-chemical basis of voltage-dependent molecular gating mechanisms in biological membranes.

The possible nature and theoretical treatment of electric field-induced molecular processes in a membrane are examined. Special attention is given to fairly fast switching phenomena as reflected by asymmetry currents as well as ionic gating in squid axon and similar systems. The apparent charge displacement associated with the underlying mechanisms is argued to be brought about by conformational transitions of integral macromolecular structures. Under these circumstances, voltage changes can actaully control the functional state of membranes by direct interference with conformational equilibria. A basic model is quantitatively discussed and shown to account for certain observed asymmetry currents. Effects due to temperature, pressure, or chemical interactions can be readily described. It is indicated how more complicated voltage-dependent membrane processes may be approached along these lines.

Animals↗
PubMed1978

Quantitative analysis of activation and inactivation of asymmetry currents in biological membranes, based on a conformational transition model.

A basic voltage-dependent conformational transition mechanism is proposed. It comprises one relatively fast conversion between two individual states which are comparatively slowly coupled with a third state. Having introduced voltage as an additional parameter of state, standard methods of thermodynamics and rate theory are employed to describe the equilibrium and kinetic behavior of the system. In particular, a quantitative discussion is given regarding the asymmetrical displacement currents generated by switching on and off a voltage pulse. Effects of temperature, pulse duration, and application of a conditioning prepulse are examined. The results provide a comprehensive basis for a quantitative analysis of pertinent experimental work. The so far presented measuring data can indeed by very well described along these lines.

Animals↗
PubMed1980

Small-signal analysis of K+ conduction in squid axons.

The maximum potential displacement that gives a linear K conductance response was determined to be 1 mV (rms) from a voltage-clamp analysis of TTX treated axons. For perturbations below this amplitude the K conductance kinetics are indistinguishable from a first-order rate process. Linearity and order of kinetics were assessed by four types of measurements: (i) the shape of the onset of the potassium current (sigmoidal vs. exponential); (ii) the symmetry of small hyperpolarizing and depolarizing pulses, (iii) wide band admittance, and (iv) harmonic analysis. The simplest interpretation of the results is that the small-signal linear response arises from a first-order gating mechanism, whereas the large-signal conventional voltage-clamp pulse of tens of millivolts evokes nonlinear phenomena. The small-signal results are consistent with the Hodgkin-Huxley description or any other nonlinear model which fits the large signal data and produces a linear first-order response for small perturbations.

Animals↗
PubMed1975

Determination of the resistance in series with the membranes of giant axons.

Measurements of the resistance in series with the excitable membrane for giant axons of two different phylla (the squid Loligo pealii and the marine worm Myxicola infundibulum) were obtained. Efforts were made to take into account the errors introduced by the finite rise-time of the measuring apparatus. The series resistance value, obtained very quickly by the method described, may be used in setting the compensation potentiometer to offset this resistance in voltage-clamp measurements. Estimates of the resistance of the periaxonal tissue layer were made. Analyses were done on some of the problems involved in attempting to make an unambiguous determination of the series resistance.

Animals↗
PubMed1979

K+ conduction phenomena applicable to the low frequency impedance of squid axon.

The observation of peaking in power spectra of K current noise in squid axon (Fishman, H.M, Moore, L.E., Poussart, D.J.M. 1975, J. Membrane Biol. 24:305) led to the calculation of low frequency K conduction feature in the impedance (admittance) which was confirmed (Fishman, H.M., Poussart, D.J.M., Moore, L.E. & Siebenga, E., 1977, J. Membrane Biol. 32:255). This paper analyzes two physical phenomena, one within and the other outside of the excitable membrane, that might account for the low frequency impedance (admittance) feature. The accumulation of potassium ions in a space outside the axon in conjunction with diffusion through the Schwann cell layer produces a low-frequency mode that is similar in some respects to that observed experimentally. Alternatively, a hypothetical inactivation process, with a voltage-dependent time constant, associated with conduction in potassium channels gives a better account of the data. Either or both of these phenomena could be involved in producing the low-frequency impedance behavior in the squid axon.

Animals↗