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M S Brodwick

Publications and source records attributed to M S Brodwick.

31 records · Page 2Linked to original sources
PubMed1981

Cyclic AMP-stimulated chloride fluxes in dialyzed barnacle muscle fibers.

Unidirectional chloride efflux and influx were studied in giant barnacle muscle fibers that were internally dialyzed. When cyclic 3'5'-adenosine monophosphate (cAMP) was included in the dialysis fluid, both unidirectional fluxes were stimulated by about the same amount. This stimulation was not associated with measurable changes either in membrane electrical conductance or with net movements of chloride. The stimulation required the trans-side presence of chloride. The stimulated flux was inhibited by the sulfonic acid stilbene derivatives 4-acetamido-4'-isothiocyanostilbene-2',2'-disulfonate (SITS) and 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) or by furosemide. When cAMP was presented in high concentrations (10-5 M), the effect on chloride fluxes was characterized by a desensitization phenomenon. This desensitization was not the result of an increased amount of phosphodiesterase activity, but may be related to ATP and/or intracellular calcium levels. These results further support the hypothesis that the barnacle sarcolemma possesses a specialized chloride transport mechanism that largely engages in Cl-Cl exchange under conditions of normal intracellular pH.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1980

Asymmetry of the acetylcholine channel revealed by quaternary anesthetics.

Tissue-cultured rat myoballs were examined electrophysiologically with a suction pipette, which was used for voltage clamping and internal perfusion. The lidocaine derivative QX-314 caused a time- and membrane potentia-dependent block of acetylcholine-induced current only when applied from the extracellular membrane surface. The same compounds caused a use-dependent block of the sodium channel only from the intracellular membrane surface. These experiments demonstrate a fundamental asymmetry of the acetylcholine receptor-channel complex.

Acetylcholine↗
PubMed1980

Acetylcholine-induced current in perfused rat myoballs.

Spherical "myoballs" were grown under tissue culture conditions from striated muscle of neonatal rat thighs. The myoballs were examined electrophysiologically with a suction pipette which was used to pass current and perfuse internally. A microelectrode was used to record membrane potential. Experiments were performed with approximately symmetrical (intracellular and extracellular) sodium aspartate solutions. The resting potential, acetylcholine (ACh) reversal potential, and sodium channel reversal potential were all approximately 0 mV. ACh-induced currents were examined by use of both voltage jumps and voltage ramps in the presence of iontophoretically applied agonist. The voltage-jump relaxations had a single exponential time-course. The time constant, tau, was exponentially related to membrane potential, increasing e-fold for 81 mV hyperpolarization. The equilibrium current-voltage relationship was also approximately exponential, from -120 to +81 mV, increasing e-fold for 104 mV hyperpolarization. The data are consistent with a first-order gating process in which the channel opening rate constant is slightly voltage dependent. The instantaneous current-voltage relationship was sublinear in the hyperpolarizing direction. Several models are discussed which can account for the nonlinearity. Evidence is presented that the "selectivity filter" for the ACh channel is located near the intracellular membrane surface.

Acetylcholine↗
PubMed1980

Effects of barium on the potassium conductance of squid axon.

Ba++ ion blocks K+ conductance at concentrations in the nanomolar range. This blockage is time and voltage dependent. From the time dependence it is possible to determine the forward and reverse rate constants for what appears to be an essentially first-order process of Ba++ interaction. The voltage dependence of the rate constants and the dissociation constants place the site of interaction near the middle of the membrane field. Comparison of the efficacy of Ba++ block at various internal K+ concentrations suggests that Ba++ is probably a simple competitive inhibitor of K+ interaction with the K+ conductance. The character of Ba++ block in high external K+ solutions suggests that Ba++ ion may be "knocked-off" the site by inward movement of external K+. Examination of the effects of other divalent cations suggests that the channel may have a closed state with a divalent cation inside the channel. The relative blockage at different temperatures implies a strong interaction between Ba++ and the K+ conductance.

Animals↗
PubMed1980

Effect of protein cross-linking reagents on membrane currents of squid axon.

The effects of the protein cross-linking reagents glutaraldehyde, tannic acid, and formaldehyde were examined in voltage-clamped and internally perfused squid axons. All three reagents reduced sodium and potassium currents and reduced or abolished sodium inactivation. Glutaraldehyde and tannic acid produced an alteration of potassium current kinetics.

Action Potentials↗
PubMed1979

Properties of chloride transport in barnacle muscle fibers.

Unidirectional chloride-36 fluxes were measured in internally dialyzed barnacle giant muscle fibers. About 50--60% of the Cl efflux was irreversibly blocked by the amino-group reactive agent, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid (SITS), when it was applied either intra- or extracellularly. Similarly, Cl influx was also blocked by SITS. No significant effect on [Cl]i of SITS was noted in intact muscle fibers. However, the rate of net Cl efflux from muscle fibers which were Cl-loaded by overnight storage at 6 degrees C could be slowed by SITS treatment. Two classes of anions were defined based upon their effects on Cl efflux. Methanesulfonate and nitrate inhibited Cl efflux either when they replaced external chloride or when they were added to a constant external chloride concentration. The other group of anions (propionate, formate) stimulated both Cl efflux and influx and such stimulation could be blocked by SITS. Propionate influx was not nearly as large as the stimulated Cl efflux and was unaffected by SITS. Neither the effects of SITS nor those of the anion substitutes could be simply accounted for by changes in the membrane resting potential or conductance. These results suggest a mediated transport system for chloride across the barnacle sarcolemma.

Animals↗
PubMed1978

Sodium channel inactivation in squid axon is removed by high internal pH or tyrosine-specific reagents.

In squid axon, internal alkalinization from pH 7.1 to pH 10.2 results in a reversible decrease of the maximum inward current and the steady state sodium channel inactivation. Similar effects were observed after treatment of the axon with tetranitromethane or after iodination with lactoperoxidase. These results suggest that a tyrosine residue is an essential component of the inactivation process in this nerve.

Animals↗
PubMed1977

Intracellular calcium and extra-retinal photoreception of Aplysia Giant neurons.

The early or "instantaneous" current-voltage relationship for the light-activated potassium current in Aplysia giant neurons was linear during the first second of illumination. However, the light current was greatly reduced or abolished by prolonged hyperpolarization. It was also greatly reduced by the injection of calcium EGTA buffers having calcium activities of 5.6 X 10(-8) M and simulated by injecting buffers with calcium activities of 2.8-5.6 X 10(-7) M. Removal of calcium from the extracellular fluid had no effect. Both the light- and calcium-activated outward potassium currents were reduced by tetraethylammonium (TEA) ions. The light current was not affected by substituting rubidium for potassium nor by substituting either lithium or Tris for sodium. The calcium-activated potassium current persisted when the neuron was cooled to 5 degrees C. However, the light response could no longer be elicited. Light hyperpolarizes Aplysia neurons probably by increasing intracellular calcium activity two-to six-fold which activates a membrane potassium conductance. Calcium levels appear to be restored within the cell and are energy dependent. The light-activated release of calcium is inhibited by cooling. The body wall of Aplysia transmits enough visible or 500 nm light to hyperpolarize some Aplysia giant neurons under ambient conditons. These neurons may be involved in the extraretinal light entrainment that occurs in Aplysia.

Animals↗
PubMed1977

Effects of nystatin on membrane conductance and internal ion activities in Aplysia neurons.

Two methods were used to study effects of the antibiotics, nystatin, on giant neurons of Aplysia. In the first method the effects of various concentrations of nystatin on the current-voltage relationship were evaluated at a fixed time after exposure to the antibiotic using a two-microelectrode voltage clamp. Nystatin increased membrane conductance in a dose-dependent manner. The dose-response relation was very steep, with little or no effect below 15 mg/liter and an effect too large to measure at concentrations greater than 30 mg/liter. Upon return to antibiotic-free solution, membrane conductance returned to pre-treatment levels within 30 minutes. The second type of experiment involved use of ion-specific microelectrodes to measure changes of intracellular univalent ion activities which attended the nystatin-induced permeability. Nystatin-induced permeability changes mainly involved univalent cations, but Cl permeability was also increased. Nystatin may therefore be used to selectively rearrange the internal ionic milieu to study the effect of such a change on membrane transport or electrical properties.

Animals↗
PubMed1975

Mechanism of action of a new toxin from gonyaulax tamarensis on nerve membranes.

The toxin from the dinoflagellate Gonyaulax tamarensis blocks nervous conduction through a selective inhibition of the mechanism whereby the membrane undergoes an increase in permeability to sodium ions. The effect is exerted only from outside of the nerve membrane. These effects are exactly the same as those exerted by tetrodotoxin or saxitoxin.

Animals↗
PubMed1972

Post-stimulus hyperpolarization and slow potassium conductance increase in Aplysia giant neurone.

1. Intracellular records from Aplysia giant (R2) cell somata showed long lasting 4-10 mV hyperpolarizations after passage of outward current through a second intracellular electrode.2. An increase in membrane slope conductance occurred simultaneously with the post-stimulus hyperpolarization (PSH).3. Both the PSH and conductance-increase varied strongly with stimulus amplitude and duration.4. Both the PSH and the conductance increase occurred in Ca-free medium containing tetrodotoxin, when action-potential production was completely blocked.5. The PSH persisted in the presence of ouabain or DNP, with cooling, with removal of external K(+), and in media where all the Na(+) was replaced with Li(+), suggesting that it was not due to the activity of an electrogenic pump.6. A reversal potential for the PSH was demonstrated by application of maintained inward current following the end of an outward-directed stimulus.7. The PSH reversal potential varied with [K](o), but not with [Cl](o) or [Na](o), suggesting that the PSH was mainly due to an increase in K conductance.8. The PSH and the conductance increase were reduced strongly when all the Na(+) was replaced with Tris, and only slightly when Na(+) was replaced with sucrose.

Action Potentials↗