Effects of lanthanum and calcium on chronically denervated muscle fibers

Parsons, R. L.; Johnson, E.; Dh, Lambert

doi:10.1152/ajplegacy.1971.220.2.401

Cited by 11 publications

(4 citation statements)

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“…Thus, similar to the effects produced by high concentrations of calcium (Ishiko and Sat0 1957), addition of lanthanum reduced the amplitude, the rate of rise, and the rate of repolarization of the action potential causing an increase in the duration of the action potential. Qualitatively similar effects of lanthanum have been observed in barnacle muscle (Hagiwara and Takahashi 1967), denervated frog muscle (Parsons, Johnson and Lambert 1971), lobster axon (Takata et al 1966, Blaustein and Goldman 1968, Hafemann 1969, and squid axon (&ore et al 1966). It is reasonable to assume that calcium governs the sodium and potassium conductances by its binding to strategic sites in the membrane, and that excitation is based on a momentary dislocation of this calcium (Frankenhaeuser and Hodgkin 1957).…”

Section: Discussionsupporting

confidence: 53%

“…In accordance with this view, it has been shown that much lower concentration> of lanthanum than of calcium (concentration ratio approximately 1 : 10-1 : 100) are required to produce a given reduction in the sodium conductance in the lobster axon (Takata et al 1966) and in the rate of rise of the action potential in denervated frog muscle (Parsons et al 1971). The strong affinity for lanthanum is further indicated by the present results which showed that even 0.5 m M lanthanum is sufficient to produce complete block of excitation in single muscle fibres.…”

Section: Discussionmentioning

confidence: 84%

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Effects of Lanthanum on the Coupling between Membrane Excitation and Contraction of Isolated Frog Muscle Fibres

Andersson

Edman

1974

Acta Physiologica Scandinavica

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The effects of lanthanum on the electrical and mechanical activities of isolated muscle fibres from the frog were investigated. Lanthanum, in the range 0.05–0.3 mM, produced characteristic, concentration dependent changes of the isometric twitch. There was an increase in latent period, increase in rate of tension development, potentiation of peak twitch amplitude, and a prolongation of the relaxation period. Lanthanum produced no change of the resting potential, hut caused a graded reduction in rate of rise, amplitude, and rate of fall of the action potential. At concentrations of the metal ion exceeding 0.3 mM, the mechanical response was complicated by impaired excitation, leading to a diminution of the twitch response and failure to produce a fused tetanus. Exposure to still higher concentrations of lanthanum (≥ 0.5 mM) made the fibre electrically inexcitable. The lanthanum‐induced changes were completely reversible on removal of the metal ion from the bath. Lanthanum in a concentration of 0.1 mM could be used as a substitute for calcium to maintain a normal resting membrane potential and twitch response. The results suggest that lanthanum and calcium act on a common site in the membrane. The alterations in twitch kinetics produced by lanthanum are discussed in relation to changes of action potential and mechanical threshold.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 84%

Effects of Lanthanum on the Coupling between Membrane Excitation and Contraction of Isolated Frog Muscle Fibres

Andersson

Edman

1974

Acta Physiologica Scandinavica

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“…The curve in Figure 3 is a computer fit to the data points and represents the sum of the two exponential expressions shown below, T/2(t) = 21.6 etll 17 + 35 e-'/58'l where t= minutes. (Manthey, 1970;Parsons, Johnson & Lambert, 1971;Cochrane & Parsons, 1972). In these instances, simultaneous perfusion of these agents with carbachol is sufficient to influence desensitization rate.…”

Section: Resultsmentioning

confidence: 99%

Effect of Ionophore X‐537a on Desensitization Rate and Tension Development in Potassium‐depolarized Muscle Fibres

DeBassio

Parsons

Schnitzler

1976

British J Pharmacology

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I The effects of the ionophore X-537A were studied on carbamylcholine (carbachol)-induced desensitization and on tension development in relaxed potassium-depolarized frog sartorius muscles. 2 X-537A accelerated carbachol-induced desensitization in Ca2+-deficient solutions without having any effect on the conductance of the membrane in the absence of carbachol or on the extent of the carbachol-induced increase in conductance. 3 In Ca2+-deficient solution, the acceleration of desensitization by the ionophore was concentrationdependent. No effect was observed with concentrations less than 5,M and maximal acceleration was evident with 10 gM. 4 The influence of X-537A on desensitization was time-dependent. At 20 AM X-537A, there was a marked acceleration of desensitization by the end of 5 min exposure. An additional gradual acceleration occurred during a 5 to 30 min treatment. No acceleration of desensitization was evident when X-537A was simultaneously applied with carbachol to the end-plate region without prior exposure to the ionophore. 5 Desensitization also was accelerated by 30 min exposure to 20 gM X-537A in solutions containing Ca2+ or deficient in both Mg2+ and Ca2+; the rate being increased 2.8-fold in Ca2+-containing solutions, 2.9-fold in Ca2+-deficient solutions containing Mg2+, and 2.5-fold in divalent cation-deficient solutions. 6 Tension development gradually occurred in relaxed potassium-depolarized muscle preparations exposed to 20 gM X-537A. The onset of tension development occurred only after approximately 25 min of exposure both in preparations kept in Ca2+-deficient or Ca2+-containing solutions. By the end of 90 min in the ionophore, the tension developed was approximately 12% and 23% of the initial potassium contracture in those preparations maintained in the Ca2+-deficient or Ca2+-containing solutions, respectively. 7 We assume that the increase in desensitization rate following exposure to X-537A results from an elevation of the intracellular Ca2+ concentration. That muscle tension gradually increased during exposure to the ionophore supports this conclusion. The acceleration of desensitization by X-537A in the absence of external Ca2+ supports the view that the site of calcium acceleration is not on the external surface of the end-plate membrane either at or near the agonist-recognition site but rather on the inner surface.

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“…For example, Parsons and Nastuk (1969) suggested that the CARB contractures which occur in potassium depolarized muscles (only in the presence of calcium) were due to an influx of calcium locally at the end plate during receptor activation. It has also been shown that CARB-induced contractures can be produced in depolarized, denervated muscle and that extracellular calcium is required (Jenkinson and Nicholls, 1961;Parsons et al, 1971). Direct evidence that the permeability to calcium is increased by ACh is derived from the work of Takeuchi (1963) and Katz and Miledi (1969).…”

Section: The Influence Of Calcium On Membrane Resistance In the Absence Of Carbmentioning

confidence: 99%

The Interaction between Caffeine and Calcium in the Desensitization of Muscle Postjunctional Membrane Receptors

Cochrane

Parsons

1972

The Journal of General Physiology

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The interaction between caffeine and calcium on the rate of desensitization of muscle postjunctional membrane (PJM) receptors during the sustained application of 0.27 mM carbamylcholine (CARB) has been studied in vitro on the sartorius muscle of the frog. The rate of PJM repolarization with CARB added to the solution bathing the muscle or the recovery of the effective transmembrane resistance (EMR) during the microperfusion of CARB directly onto the end-plate region of individual fibers was used as an index of the rate of desensitization. Caffeine (1.5 m) increased the rate of PJM repolarization with bulk application of CARB in a 1.8 or 10 mm calcium Ringer solution but had no effect on PJM repolarization in a calcium-deficient, 4 mmu magnesium Ringer solution. For EMR measurements the preparation was rendered mechanically quiescent by repeated challenges with isotonic KC1 during an exposure of several hours to a calcium-free, 4 mM magnesium-l mm EGTA Ringer solution. In these fibers, the microperfusion of 0.27 mu CARB together with 1.8 mM calcium plus 1.5 mM caffeine significantly increased the rate of EMR recovery above that observed in the absence of caffeine. Raising the calcium concentration to 10 mM had a similar effect; however, no additional increase was noted by the inclusion of 1.5 mM caffeine. It is suggested that the major role of caffeine in PJM desensitization is to increase the calcium permeability of the surface membrane. The transmembrane movement of calcium and the consequent intracellular accumulation of calcium is seen as a critical factor in controlling the rate of PJM desensitization.

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Effects of lanthanum and calcium on chronically denervated muscle fibers

Cited by 11 publications

References 0 publications

Effects of Lanthanum on the Coupling between Membrane Excitation and Contraction of Isolated Frog Muscle Fibres

Effects of Lanthanum on the Coupling between Membrane Excitation and Contraction of Isolated Frog Muscle Fibres

Effect of Ionophore X‐537a on Desensitization Rate and Tension Development in Potassium‐depolarized Muscle Fibres

The Interaction between Caffeine and Calcium in the Desensitization of Muscle Postjunctional Membrane Receptors

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