scholarly journals Calcium and potassium systems of a giant barnacle muscle fibre under membrane potential control

1973 ◽  
Vol 229 (2) ◽  
pp. 409-455 ◽  
Author(s):  
R. D. Keynes ◽  
E. Rojas ◽  
R. E. Taylor ◽  
J. Vergara
1982 ◽  
Vol 98 (1) ◽  
pp. 39-47
Author(s):  
P. J. Stephens ◽  
H. L. Atwood

1. Effects of temperature on the muscle fibre membrane and synapses of stretcher muscle preparations made from autotomized limbs of the Pacific shore crab (Pachygrapsus crassipes) were investigated. 2. Acclimation of the crabs to different temperatures modified properties of both muscle fibre membrane and synapses. 3. Increased temperature produced an increase in membrane potential of the muscle fibres. A semi-log plot of these data revealed two linear phases of the membrane potential-temperature relationship, with a change in slope near the acclimation temperature. 4. Maximum values for excitatory junction potential (EJP) amplitude and time constant of EJP decay, and minimum values for facilitation were obtained at temperatures close to the acclimation temperature. It is suggested that the decline in EJP amplitude and time constant of decay produced by deviations in temperature from the acclimation temperature is compensated for by an increase in the amount of facilitation. In this way, maximum tension can be produced by the stretcher muscle in a range of at least 8 degrees C around the acclimation temperature.


1983 ◽  
Vol 244 (3) ◽  
pp. C297-C302 ◽  
Author(s):  
S. S. Sheu ◽  
M. P. Blaustein

The influence of internal and external Ca2+ on membrane potential and 22Na influx were tested in internally perfused giant barnacle muscle fibers. The fibers depolarized by about 2-3 mV, and Na+ influx increased when external Ca2+ was removed. These effects were inhibited and reversed by adding 2 mM La3+ externally but not by tetrodotoxin (TTX). Ca2+ channel blockers did not prevent the depolarization. Increasing internal free Ca2+ ([Ca2+]i) from 10(-7) to 10(-5) M also stimulated Na+ influx and depolarized the fibers by a few millivolts. Neither external La3+ nor TTX prevented the effects of raising [Ca2+]i; however, internal tetrabutylammonium ions depolarized the fibers and attenuated the internal Ca2+-dependent effects. These data are consistent with the idea that removal of external Ca2+ activates a La3+-sensitive channel that is permeable to Na+; raising [Ca2+]i activates a La2+-insensitive, Na+-permeable channel that may be similar to the internal Ca2+-activated nonselective cation channels observed in cardiac muscle. The results demonstrate that all Na+ (and Ca2+) fluxes that do not contribute to Na-Ca exchange must be carefully identified before the exchange stoichiometry can be determined from Na+ and Ca2+ flux measurements.


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