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PubMed1970

Photo-affinity labeling of specific acetylcholine-binding sites on membranes.

Acetylcholinesterase of intact red blood cell membranes and the acetylcholine receptor at the neuromuscular junction of whole-frog sartorius muscle have been irreversibly inactivated by photo-affinity labeling with two quaternary ammonium aryl azides. The inactivation requires that the azides, at the time of their photolytic conversion to highly reactive nitrenes, are reversibly bound to the specific acetylcholine-binding sites.

Acetylcholine↗
PubMed1978

Blockade of neuromuscular transmission by enzymatically active and inactive beta-bungarotoxin.

beta-Bungarotoxins have been shown to be presynaptic blockers of neuromuscular transmission. This paper reports experiments using the most positively charged beta-bungarotoxin that elutes from a CM-Sephadex C-25 column. The toxin is shown to be a single polypeptide with a molecular weight of approximately 11,000 and has phospholipase A2 activity. The application of the enzymatically active toxin to the frog sciatic nerve-sartorius muscle preparation results in an initial decrease in the average endplate potential amplitude followed by a temporary rebound in endplate potential amplitude, and finally a complete inhibition of endplate potentials. Similarly, minature endplate potential frequency is initially reduced upon toxin application but then increases dramatically. After the phospholipase A2 of the toxin is inactivated, treatment with the toxin results in only the initial decrease in transmitter release. There results suggest that this beta-bungarotoxin acts in two functionally separate steps: (i) by binding to a specific presynaptic site possibly associated with calcium entry, and (ii) by perturbing the presynaptic membrane by its enzyme action, which results in an increase and then a failure in transmitter release.

Action Potentials↗
PubMed1979

Tetraethylammonium: voltage-dependent action on endplate conductance and inhibition of ligand binding to postsynaptic proteins.

Tetraethylammonium (Et(4)N(+)) ions depressed the amplitude and accelerated the decay rate of spontaneously occurring and nerve-evoked endplate currents (EPCs) in frog sartorius muscle. The relationship between peak EPC amplitude and membrane potential became nonlinear in the presence of 100 muM Et(4)N(+), and with drug concentrations of 250 muM or greater the current-voltage relationship exhibited negative conductance in the hyperpolarized region. Et(4)N(+) modified the exponential dependence of the EPC decay on membrane potential such that the decays between -150 and -50 mV were abbreviated and voltage independent but remained near control levels at more positive membrane potentials. The minimal effective concentration of Et(4)N(+) for altering the EPC time course was 10, and maximal effects were attained with 100 muM. Little additional shortening in the EPC decay phase was detected on raising the drug concentration to 1000 muM. Acetylcholine noise analysis revealed a voltage-dependent reduction in the mean channel open time, which was comparable in magnitude to the shortening in the EPC decay, and a depression of single-channel conductance. In concomitant biochemical studies, Et(4)N(+) was found to inhibit the binding of both [(3)H]acetylcholine and [(3)H]perhydrohistrionicotoxin to receptor-rich membranes from the electric organ of Torpedo ocellata with K(i) values of 200 muM and 280 muM, respectively. These results suggest that Et(4)N(+) interacts with both the acetylcholine receptor and its associated ionic channel. The voltage-dependent actions of Et(4)N(+) are attributed to blockade of the ionic channel in closed as well as open conformation.

Acetylcholine↗
PubMed1980

[3H]Phencyclidine: a probe for the ionic channel of the nicotinic receptor.

To evaluate [3H]phencyclidine ([3H]PCP)as a probe for the ionic channel of the nicotinic receptor, the characteristics of its binding to electric organ membranes od Torpedo ocellata and its effects on frog sartorius muscle were studied. Similar to PCP, [3H]PCP depressed the peak amplitude of endplate current, caused nonlinearity in the voltage-current relationship at negative potentials, accelerated the decay time of the end-plate current, and shortened the channel lifetime. Thus, [3H]PCP interacted with the ionic channel of the nicotinic receptor, although there were a few differences between its effect and that of PCP. Binding of [3H]PCP to Torpedo membranes was to sites on the ionic channel of acetylcholine (AcCho) receptor because it was saturable, dependent upon protein concentration, and inhibited by drugs that interact with the ionic channel, and the initial rate of binding was potentiated by receptor agonists. Equilibrium binding of [3H]PCP to Torpedo membranes was with two affinities, but in the presence of AcCho, [3H]PCP binding was with a single affinity. The affinities of channel drugs obtained by inhibition of binding of [3H]PCP and [3H[perhydrohistrionicotoxin to Torpedo membranes were different, with correlation coefficients of 0.52 and 0.82 in the absence and presence of a receptor agonist, respectively; this suggests differences in their binding sites on the ionic channel of the AcCho receptor.

Animals↗
PubMed2003

Introduction of exogenous DNA into gonads of chick embryos by lipofection and electroporation of stage X blastoderms in vivo.

1. In order to introduce exogenous DNA into gonads of chick embryos, stage X blastoderms of freshly laid and unincubated eggs were transfected by lipofection and electroporation in vivo. 2. The introduced DNA, green fluorescence protein (GFP) gene, was efficiently expressed in the blastoderms incubated for 24 h (78.8%, 78/99). 3. The GFP gene was present in most of the embryonic bodies and extra-embryonic membranes died by d 10 of incubation, when analysed by polymerase chain reaction. On d 16 to 20 of incubation, the GFP gene was detected in 7.0 to 20.9% of embryos in the heart, liver, stomach and brain, but not in the sartorius muscle. For the gonads, the GFP gene was detected in 22.2% (6/27) of the testes and 6.3% (1/18) of the ovaries examined. 4. These results suggest that it is possible to introduce exogenous DNA into gonads of chick embryos by lipofection and electroporation of stage X blastoderms in vivo.

Animals↗
PubMed1963

On the structural continuities of the transverse tubular system of rabbit and human myocardial cells.

An electron microscopic study of rabbit and human myocardium provides further evidence of the existence of two distinct components of the sarcoplasmic reticulum. A thin-walled tubular system (termed longitudinal system) is arranged in anastomosing channels sur-surrounding each sarcomere and has transverse and possibly also longitudinal connections with the tubules of adjacent sarcomeres. A thick-walled tubular system traverses the myofiber transversely at the level of the Z lines of the myofibrils. The structure of these tubules very closely resembles that of deep sarcolemmal invaginations. Indeed, the membranes of the tubules appear to be continuous with the sarcolemma in favorable sections so that there seems to be an extension of the cell membrane and extracellular fluid to all depths of the myocardial fiber. Certain physiologic data which support this concept are discussed. The calculations of A. V. Hill comparing the kinetics of diffusion and the time-distance relationships between excitation and activation in frog sartorius muscle are reconsidered for cardiac muscle.

Animals↗
PubMed1973

Evidence for recycling of synaptic vesicle membrane during transmitter release at the frog neuromuscular junction.

When the nerves of isolated frog sartorius muscles were stimulated at 10 Hz, synaptic vesicles in the motor nerve terminals became transiently depleted. This depletion apparently resulted from a redistribution rather than disappearance of synaptic vesicle membrane, since the total amount of membrane comprising these nerve terminals remained constant during stimulation. At 1 min of stimulation, the 30% depletion in synaptic vesicle membrane was nearly balanced by an increase in plasma membrane, suggesting that vesicle membrane rapidly moved to the surface as it might if vesicles released their content of transmitter by exocytosis. After 15 min of stimulation, the 60% depletion of synaptic vesicle membrane was largely balanced by the appearance of numerous irregular membrane-walled cisternae inside the terminals, suggesting that vesicle membrane was retrieved from the surface as cisternae. When muscles were rested after 15 min of stimulation, cisternae disappeared and synaptic vesicles reappeared, suggesting that cisternae divided to form new synaptic vesicles so that the original vesicle membrane was now recycled into new synaptic vesicles. When muscles were soaked in horseradish peroxidase (HRP), this tracerfirst entered the cisternae which formed during stimulation and then entered a large proportion of the synaptic vesicles which reappeared during rest, strengthening the idea that synaptic vesicle membrane added to the surface was retrieved as cisternae which subsequently divided to form new vesicles. When muscles containing HRP in synaptic vesicles were washed to remove extracellular HRP and restimulated, HRP disappeared from vesicles without appearing in the new cisternae formed during the second stimulation, confirming that a one-way recycling of synaptic membrane, from the surface through cisternae to new vesicles, was occurring. Coated vesicles apparently represented the actual mechanism for retrieval of synaptic vesicle membrane from the plasma membrane, because during nerve stimulation they proliferated at regions of the nerve terminals covered by Schwann processes, took up peroxidase, and appeared in various stages of coalescence with cisternae. In contrast, synaptic vesicles did not appear to return directly from the surface to form cisternae, and cisternae themselves never appeared directly connected to the surface. Thus, during stimulation the intracellular compartments of this synapse change shape and take up extracellular protein in a manner which indicates that synaptic vesicle membrane added to the surface during exocytosis is retrieved by coated vesicles and recycled into new synaptic vesicles by way of intermediate cisternae.

Animals↗
PubMed1981

Absence of filipin-sterol complexes from the membranes of active zones and acetylcholine receptor aggregates at frog neuromuscular junctions.

The polyene antibiotic filipin reacts specifically with membrane cholesterol and produces distinctive membrane lesions. We treated frog cutaneous and sartorius muscles with 0.04% filipin in a glutaraldehyde solution with or without prefixation with glutaraldehyde. Freeze-fracture of these muscles revealed numerous 19 to 38-nm protuberances and depressions (filipin-sterol complexes) in most areas of muscle, axon, and Schwann cell membranes. In the presynaptic membrane, however, these filipin-sterol complexes were absent from active zones consisting of ridges bordered with double rows of particles. In the postsynaptic membrane, filipin-sterol complexes were also virtually absent from the areas occupied by aggregates of large particles representing acetylcholine receptors. These results suggest that the membrane regions of active zones and acetylcholine receptor aggregates have a low cholesterol content.

Animals↗
PubMed1956

The non-correlation of bioelectric potentials with ionic gradients.

The sartorius muscles of 320 toads have been analyzed for Na(+) and K(+). There is a wide variation in the Na(+) content which when calculated intracellularly varied from 0 m.eq./kg. to 58 m.eq./kg. In particular it was found that the distribution of internal Na(+) in the intact animal was such that only 17 per cent of the muscles should give from the Nernst equation the observed overshoot of 37 mv. In contrast to this wide variation the K(+) content is comparatively constant, the range being 71 to 112 m.eq./kg. The mean observed resting potential of 87 mv. agreed well with the potential calculated from the mean intracellular K(+) by the Nernst equation. Analyses of plasma show that the Na(+) content is constant at 130 m.eq./liter, and the K(+) is 3.0 m.eq./liter. The resting and action potentials of 77 muscles have been recorded and then the muscles have been analyzed. The results have shown that there is no correlation between the level of intracellular Na(+) and the overshoot. Furthermore the apparent correlation between the average K(+) content and the average resting potential has been shown to be fortuitous, when the correlation in individual muscles is considered. When a muscle is soaked in Ringer solution for several hours there is a gain of Na(+) and a loss of K(+). These shifts should result in changes in the respective potentials, but such changes were not found. The above findings have been discussed in the light of the present theories that the resting potential and the action potential are directly related to the ionic ratio across the membrane. Our results very definitely do not support the theory that the overshoot is related to the Na(+) gradient, and this also applies with respect to the K(+) gradient and the resting potential.

Action Potentials↗
PubMed1963

Total energy production and phosphocreatine hydrolysis in the isotonic twitch.

Using frog's sartorius muscles we have found no correlation between phosphocreatine hydrolysis and shortening under conditions (iodoacetate poisoning and anoxia) where this reaction was the only expected source of energy. Phosphocreatine hydrolysis did, however, show a constant term corresponding to the activation heat of A.V. Hill, and a linear term with work. It was concluded that shortening heat comes from some other chemical reaction, or else Hill's equation (E = A + W + ax) fails to describe correctly the energy output in a complete cycle of contraction and relaxation. To decide between these possibilities direct measurements of heat and work during a complete cycle were made. Also, experiments were performed in which heat, work, and phosphocreatine breakdown were measured simultaneously on the same muscles. The total energy output in a complete twitch could be most simply represented by a fixed "activation" heat, plus the work. There was no term corresponding to the shortening heat. Hill's equation must, therefore, be held as invalid for the complete isotonic twitch. A value of 9.8 +/- 0.5 (sE) kcal/mole was obtained for the in vivo heat of hydrolysis of phosphocreatine. This quantity showed no significant dependence on load, and it is in good agreement with the value obtained from thermochemical data. It is concluded that phosphocreatine hydrolysis and its associated buffer reactions can account quantitatively for the total energy output of isometric and isotonic twitches.

Animals↗
PubMed1964

SELECTIVE INHIBITION OF POTASSIUM CONTRACTURE IN PRESENCE OF INTACT TWITCH.

If a sartorius muscle of frog is pretreated for 30 min. with a hyposmotic Ringer's (called "hyposmotic potassium chloride") in which all sodium chloride is replaced by 23 mM potassium chloride, and then is immersed in normal Ringer's for about 40 min., a twitch of normal size can be elicited although the potassium contracture is almost completely abolished. During the time that this selective inhibition of potassium contracture occurs, the action potential and both the size and the speed of depolarization due to potassium are almost the same as in a control muscle that is pretreated for 30 min. with 23 mM potassium chloride under isosmotic conditions and that can give a normal potassium contracture. If a muscle is pretreated not with hyposmotic potassium chloride but with a hyposmotic Ringer's in which the concentration of sodium chloride is reduced to 22 mM, the evoked potassium contracture is inhibited, but to a much smaller degree. The partial replacement of chloride by nitrate in hyposmotic potassium chloride has no influence on the degree of the selective inhibition. If after the pretreatment with hyposmotic potassium chloride the muscle is left in normal Ringer's for about 3 hours, there is considerable recovery of ability to undergo contracture. The mechanism of the selective inhibition is briefly discussed.

Animals↗
PubMed1969

Ionic conductances of the surface and transverse tubular membranes of frog sartorius fibers.

The resting ionic conductances of frog sartorius muscle fibers have been determined in a variety of conditions in order to measure the potassium conductance of the tubular and surface membranes (gK(t) and gK(s)) and the chloride conductance of the tubular and surface membranes (gCl(t) and gCl(s)). In both normal fibers and fibers without tubules, measurements of input resistance and diameter were made at normal pH and at low pH when the chloride conductance was very small. These measurements permitted the separation of the ionic conductances: gCl(s) = 219 micromhos/cm(2); gCl(t) = 0 micromhos/cm(2); gK(s) = 28 micromhos/cm(2); gK(t) = 55 micromhos/cm(2). Possible sources of systematic error are discussed and a statistical analysis of the effects of random error is presented. The implications of the nonuniformity of membrane properties are discussed along with possible anatomical explanations.

Animals↗
PubMed1969

Action potentials, afterpotentials, and excitation-contraction coupling in frog sartorius fibers without transverse tubules.

In frog sartorius muscle fibers in which the transverse tubular system has been disrupted by treatment with glycerol, action potentials which are unaccompanied by twitches can be recorded. These action potentials appear to be the same as those recorded in normal fibers except that the early afterpotential usually consists of a small hyperpolarization of short duration. After a train of action potentials no late afterpotential is seen even when the membrane potential is changed from the resting level. In fibers without transverse tubules hyperpolarizing currents do not produce a creep in potential. The interruption of excitation-contraction coupling, the changes in the afterpotentials, and the disappearance of creep are all attributed to the lack of a transverse tubular system.

Action Potentials↗
PubMed1973

A linear dose-response curve at the motor endplate.

The motor endplate of frog sartorius muscle was voltage clamped and the peak current to different concentrations of acetylcholine and carbachol applied in the perfusing fluid was measured. Perfusing fluid was hypertonic in order to suppress contractions. Current responses were smooth and reached a peak value within 2-5 s. The dose-response curve was usually linear even with concentrations of 10(-2) M acetylcholine, indicating that the conductance change was probably proportional to the concentration of acetylcholine or carbachol. With high concentrations nonlinearity sometimes appeared but in these cases the fast onset of desensitization appeared to be preventing the current response from reaching its expected peak amplitude. When the depolarization produced by acetylcholine in a non-voltage-clamped endplate was measured the dose-response curve was hyperbolic. This relationship was imposed by the electrical properties of the endplate membrane and its surrounding sarcolemma, and could be predicted if the input resistance of the fiber was known. Experiments were also done on slow muscle fibers. Depolarizing analogues of acetylcholine had similar effects to acetylcholine. d-Tubocurarine reduced the proportionality constant between concentration of acetylcholine and conductance change, and this resulted in a parallel shift of the log-concentration depolarization curve. A linear dose-response curve was unexpected within the context of current theories of drug action.

Acetylcholine↗
PubMed1979

The time-course of energy balance in an isometric tetanus.

Unpoisoned sartorius muscles of Rana temporaria were stimulated tetanically in isometric contractions lasting up to 20 s at 0 degrees C. The observed enthalpy (heat + work) production and the chemical changes in these contractions were measured, and a comparison was made between the observed enthalpy and the enthalpy that could be explained by the chemical changes. Like earlier workers, we found that the only net known reaction of energetic significance that occurred was dephosphorylation of n-phosphoryl creatine (PC), and we found a significant evolution of unexplained enthalpy (UE), a portion of the observed enthalpy which could not be explained by the extent of PC dephosphorylation. We measured the total quantity and the rate of production of the UE, and we found that its rate of evolution, which was most rapid during the first 750 ms of contraction, fell progressively to zero by the 8th s of contraction: i.e., after 8 s of contraction, all the observed enthalpy is adequately explained by PC dephosphorylation. The time-course of evolution of the UE was slower than that of the labile enthalpy (a component of the enthalpy evolved in isometric contraction whose rate of production declines exponentially at approximately 1 s-1). We conclude that, although the magnitudes of these enthalpy quantities may be similar, they are not derived from the same chemical reaction in muscle.

Animals↗
PubMed1979

Reaction of tetraethylammonium with the open and closed conformations of the acetylcholine receptor ionic channel complex.

The effect of tetraethylammonium (TEA) bromide on the neurally and iontophoretically evoked endplate current (EPC) of frog sartorius muscle was investigated using voltage-clamp and noise analysis techniques, and its binding to the acetylcholine (ACh) receptor ionic channel complex was determined on the electric organ of Torpedo ocellata. TEA (250-500 microM) produced an initial enhancement followed by a slow decline in the amplitude of the endplate potential and EPC, but caused only depression in the amplitude of the miniature endplate potential and current. In normal ringer's solution, the EPC current-voltage relationship was approximately linear, and the decay phase varied exponentially with membrane potential. Upon addition of 50-100 microM TEA, the current-voltage relationship became markedly nonlinear at hyperpolarized command potentials, and with 250-2000 microM TEA, there was an initial linear segment, an intermediate nonlinear segment, and a region of negative conductance. The onset of nonlinearity was dose-dependent, undergoing a 50 mV shift for a 10-fold increase in TEA concentration. The EPC decay phase was shortened by TEA at hyperpolarized but not depolarized potentials, and remained a single expotential function of time at all concentrations and membrane potentials examined. These actions of TEA were found to be independent of the sequence of polarizations, the length of the conditioning pulse, and the level of the initial holding potential. TEA shifted the power spectrum of ACh noise to higher frequencies and produced a significant depression of single channel conductance. The shortening in the mean channel lifetime agreed closely with the decrease in the EPC decay time constant. At the concentrations tested, TEA did not alter the EPC reversal potential, nor the resting membrane potential, and had little effect on the action potential duration. TEA inhibited the binding of both [3H] ACh (Ki = 200 microM) and [3H]perhydrohistrionicotoxin (Ki = 280 microM) to receptor-rich membranes from the electric organ of Torpedo ocellata, and inhibited the carbamylcholine-activated 22Na+ efflux from these microsacs. It is suggested that TEA reacts with the nicotinic ACh-receptor as well as its ion channel; the voltage-dependent actions are associated with blockade of the ion channel. The results are compatible with a kinetic model in which TEA first binds to the closed conformation of the receptor-ionicchannel complex to produce a voltage-depdndent depression of endplate conductance and sudsequently to its open conformation, giving rise to the shortening in the EPC decay and mean channel lifetime.

Acetylcholine↗
PubMed1980

Voltage dependence of desensitization. Influence of calcium and activation kinetics.

The voltage dependence of carbachol-induced desensitization has been analyzed in potassium-depolarized frog sartorius muscle preparations with voltage clamp techniques over a wide voltage range (-120 to +40 mV). Desensitization developed exponentially at all voltages with tau, the time constant of desensitization onset, varying as a logarithmic function of membrane voltage. The voltage dependence of tau remained in calcium-deficient solutions and was not altered by elevating either the level of extracellular or intracellular calcium. We have analyzed our results according to a simple sequential kinetic scheme in which the rate-limiting step in the development of desensitization is a transition of the receptor channel complex from the activated conducting state to a desensitized, nonconducting state. We conclude (a) that the observed voltage sensitivity of desensitization primarily resides in the voltage dependence of this transition, and (b) the kinetics of activation appear to have a greater influence on the observed rate of desensitization than on its voltage dependence. The magnitude of the voltage dependence suggests that a greater change in free energy is required for the transition to the desensitized state than for the transition between the open and closed states of the receptor channel complex.

Animals↗
PubMed1980

Effects of ammonium ions on endplate channels.

Miniature endplate currents, recorded from voltage-clamped toad sartorius muscle fibers in solutions containing ammonium ions substituted for sodium ions, were increased in amplitude and decayed exponentially with a slower time constant than in control (Na) solution. The peak conductance of miniature endplate currents was also greater in ammonium solutions. The acetylcholine null potential was -2.8 +/- 0.8 mV in control solution, and shifted to 0.9 +/- 1.6 mV in solutions in which NH4Cl replaced half the NaCl. In solutions containing NH4Cl substituted for all the NaCl, the null potential was 6.5 +/- 1.3 mV. Single channel conductance and average channel lifetime were both increased in solutions containing ammonium ions. The exponential relationship between the time constant of decay of miniature endplate currents or channel lifetime and membrane potential was unchanged in ammonium solutions. A slight but consistent increase in peak conductance during miniature endplate currents and single channel conductance was seen as membrane potential became more positive (depolarized) in both control and ammonium solutions. Net charge transfer was greater in ammonium solutions than in control solution, whether measured during a miniature endplate current or through a single channel. The results presented here are consistent with an endplate channel model containing high field strength, neutral sites.

Ammonium Chloride↗