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L Byerly

Publications and source records attributed to L Byerly.

26 records · Page 2Linked to original sources
PubMed1982

Slowing of sodium current inactivation by ruthenium red in snail neurons.

The effects of ruthenium red (RuR) were tested on the membrane currents of internally perfused, voltage-clamped nerve cell bodies from the snail Limnea stagnalis. Bath application of nanomolar concentrations of RuR produces a prolonged Na current that decays approximately 40 times slower than the normal Na current in these cells. The relationship between the reversal potential for the prolonged Na current and the intracellular concentration of Na+ agrees well with the constant-field equation, assuming a small permeability for Cs+. Because a strong correlation was found between the magnitude of the normal Na current and that of the prolonged Na current, it is concluded that the prolonged Na current flows through the normal Na channels. This conclusion is supported by the similar selectivities, voltage dependencies, and tetrodotoxin (TTX) sensitivities of these two currents. This action of RuR to slow the inactivation of the Na channel was not observed at concentrations below 1 nM, but was complete at 10 nM. When the concentration of RuR is increased to 0.1 mM, the Ca current in these cells is blocked; but at this high concentration RuR also reduces the outward voltage-dependent currents and resting membrane resistance. Therefore, RuR is not a good Ca blocker because of its lack of specificity. However, its action of slowing Na current inactivation is very specific and could prove to be useful in studying the inactivation of the Na channel.

Animals↗
PubMed1982

Calcium currents in internally perfused nerve cell bodies of Limnea stagnalis.

1. When K(+) is removed from both sides of the somal membrane of Limnea neurones, time-dependent, voltage-dependent outward currents are observed at positive potentials. These currents can be carried by Tris(+) and tetraethylammonium (TEA(+)), as well as Cs(+), but the Cs currents are several times larger. The Cs currents are not affected by external or internal TEA, but are strongly reduced by 4-aminopyridine (4-AP) and all Ca blockers tried.2. The presence of these non-specific outward currents and their sensitivity to all treatments that eliminate the Ca currents prevent the complete isolation of Ca currents. The non-specific outward currents are most prominent at large positive potentials and as slow tail currents on stepping back to the holding potential.3. Ca currents are ;washed out' in well perfused cells. Typically the Ca current has decayed to less than one tenth of its original size after (1/2) h of perfusion. This wash-out is specific for the Ca current; Na and K currents persist for several hours.4. Once the Ca current has completely decayed, it is possible to study one type of non-specific current without overlapping inward currents. This current activates between 0 and +30 mV and appears to reverse near 0 mV.5. In spite of the probable presence of slowly activating outward currents, the net inward currents measured show little apparent inactivation. In all the cells studied the inward current evoked at +20 mV has never decayed by more than 50% during a 60 ms pulse. So the true inactivation of these Ca currents must be quite slow, with time constants of the order of 100 ms and larger.6. The activation of the Ca current agrees with m(2) kinetics. The rate of activation is the same for Ba currents as for Ca currents.7. When the membrane potential is stepped back to the holding level (-50 mV), the Ca current turns off quite rapidly with a time constant of about 100 mus (25 degrees C). The time constant for turning off the Ca current is not related to the time constant for turning on the Ca current at the same voltage as expected for m(2) kinetics in the Hodgkin and Huxley model. At -30 mV the tau(m) for turn-on is eight times larger than the tau(m) for turn-off.

Animals↗
PubMed1981

Calcium channel.

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Action Potentials↗
PubMed1981

Membrane biophysics of calcium currents.

Voltage-dependent Ca currents have now been identified in almost every excitable membrane. In invertebrate muscle and many egg cells Ca currents produce pure Ca spikes, while in nerve axons and vertebrate skeletal muscle Ca currents contribute little to the action potential. Nerve cell bodies and secretory cells have action potentials with both Na and Ca components. Since the measurement of the Ca reversal potential is practically impossible, the selectivity of Ca channels can only be determined by the current-carrying ability of various ions. The movement of ions through the Ca channel is described in terms of an affinity factor for an external binding site and a mobility factor for crossing the membrane. The biophysical study of Ca currents has been limited by the absence of preparations where control of membrane potential was satisfactory. Recently, spherical cells such as isolated ganglion cells and egg cells have allowed more satisfactory voltage clamp studies. However, the separation of the Ca current from the background currents is a much more difficult problem than was the isolation of the Na current. This difficulty is due to the multiple interrelations between the background current and the Ca current. In general alterations that change the Ca current also appear to change the background current.

Animals↗
PubMed1979

Voltage-clamp analysis of the potassium current that produces a negative-going action potential in Ascaris muscle.

1. A voltage clamp has been developed for the pharyngeal muscle of the nematode Ascaris lumbricoides and has been used to analyse the potassium current that produces a negative-going, regenerative action potential in this muscle. 2. Depolarizing voltage steps elicit a sustained inward current; returning the membrane voltage to the resting level evokes a strong, transient, outward current. This outward current reverses direction at the same voltage as that reached by the negative-going spike and is identified as the negative spike current. 3. The negative spike current decays with a time constant of 30 msec at voltages more negative than -30mV. This inactivation of the negative spike conductance is removed by holding the membrane at potentials more positive than -15mV. The time constant for removal of inactivation decreases from more than 300 msec at -15 mV to about 30 msec at +10 mV. 4. When inactivation has been removed, the negative spike conductance is turned on by stepping to potentials more negative than -15 mV. 5. Although the reversal potential for this current depends strongly on [K+]o (42 mV/decade), the potential at which the conductance is turned on is independent of [K+]o. 6. External Na+ seems to facilitate the negative spike current. Reduction of [Na+]o reduces its conductance and shifts the reversal potential to more positive values. 7. External Rb+ and Cs+ show voltage-dependent blocking of this current. 8. This K current is different from all the K currents which have been studied previously; however, it is analogous to the classical Na current of nerve and muscle, except for an inversion of the voltage dependencies.

Action Potentials↗