Factors affecting membrane permeability and ionic homeostasis in the cold-submerged frog

2000 ◽  
Vol 203 (2) ◽  
pp. 405-414 ◽  
Author(s):  
P.H. Donohoe ◽  
T.G. West ◽  
R.G. Boutilier

Frogs (Rana temporaria) were submerged at 3 degrees C in either normoxic (P(O2)=155 mmHg, P(O2)=20 kPa) or hypoxic (P(O2)=60 mmHg; P(O2)=8 kPa) water for up to 16 weeks, and denied air access, to mimic the conditions of an ice-covered pond during the winter. The activity of the skeletal muscle Na(+)/K(+) pump over the first 2 months of hibernation, measured by ouabain-inhibitable (22)Na(+) efflux, was reduced by 30 % during normoxia and by up to 50 % during hypoxia. The reduction in Na(+)/K(+) pump activity was accompanied by reductions in passive (22)Na(+) influx and (86)Rb(+) efflux (effectively K(+) efflux) across the sarcolemma. This may be due to a decreased Na(+) permeability of the sarcolemma and a 75 % reduction in K(+) leak mediated by ATP-sensitive K(+) channels (‘K(ATP)’ channels). The lowered rates of (22)Na(+) and (86)Rb(+) flux are coincident with lowered transmembrane ion gradients for [Na(+)] and [K(+)], which may also lower Na(+)/K(+) pump activity. The dilution of extracellular [Na(+)] and intracellular [K(+)] may be partially explained by increased water retention by the whole animal, although measurements of skeletal muscle fluid compartments using (3)H-labelled inulin suggested that the reduced ion gradients represented a new steady state for skeletal muscle. Conversely, intracellular ion homeostasis within ventricular muscle was maintained at pre-submergence levels, despite a significant increase in tissue water content, with the exception of the hypoxic frogs following 4 months of submergence. Both ventricular muscles and skeletal muscles maintained resting membrane potential at pre-submergence levels throughout the entire period of hibernation. The ability of the skeletal muscle to maintain its resting membrane potential, coincident with decreased Na(+)/K(+) pump activity and lowered membrane permeability, provided evidence of functional channel arrest as an energy-sparing strategy during hibernation in the cold-submerged frog.

1979 ◽  
Vol 64 (1) ◽  
pp. 231-234 ◽  
Author(s):  
Elis F. Stanley ◽  
Daniel B. Drachman

1980 ◽  
Vol 58 (6) ◽  
pp. 600-605 ◽  
Author(s):  
C. M. Thomson ◽  
W. F. Dryden

Resting membrane potentials and membrane conductances of chick skeletal muscle in culture were determined from the 3rd to the 10th day after plating. The effect of tetraethylammonium (TEA) and of replacement of potassium with caesium on these parameters was investigated. Resting membrane potential (Em) rises during myogenesis in vitro and resting membrane conductance (Gm) falls. The initial level of Gm was relatively high (1.2 mS cm−2) but this fell to a final level around 0.2 mS cm−2. The most rapid changes in both parameters occurred between days 3 and 5 of culture. Both TEA and caesium depressed Em and Gm at all stages of development. On the 3rd day of culture Gm was reduced by 0.2 mS cm−2 by both agents. Thereafter, Gm was depressed by about 0.1 mS cm−2. Caesium does not penetrate potassium channels and the reduction in Gm is attributed to block of these channels. This indicates that resting potassium conductance is relatively constant at 0.1 mS cm−2 throughout muscle fibre development. Because TEA produces changes in Gm similar to those produced by caesium, TEA is concluded to be acting at the potassium channel in a manner similar to caesium.


2001 ◽  
Vol 153 (4) ◽  
pp. 677-686 ◽  
Author(s):  
Jacqueline Fischer-Lougheed ◽  
Jian-Hui Liu ◽  
Estelle Espinos ◽  
David Mordasini ◽  
Charles R. Bader ◽  
...  

Myoblast fusion is essential to skeletal muscle development and repair. We have demonstrated previously that human myoblasts hyperpolarize, before fusion, through the sequential expression of two K+ channels: an ether-à-go-go and an inward rectifier. This hyperpolarization is a prerequisite for fusion, as it sets the resting membrane potential in a range at which Ca2+ can enter myoblasts and thereby trigger fusion via a window current through α1H T channels.


2001 ◽  
Vol 118 (6) ◽  
pp. 653-678 ◽  
Author(s):  
S. Hollingworth ◽  
J. Peet ◽  
W.K Chandler ◽  
S.M. Baylor

Calcium sparks were studied in frog intact skeletal muscle fibers using a home-built confocal scanner whose point-spread function was estimated to be ∼0.21 μm in x and y and ∼0.51 μm in z. Observations were made at 17–20°C on fibers from Rana pipiens and Rana temporaria. Fibers were studied in two external solutions: normal Ringer's ([K+] = 2.5 mM; estimated membrane potential, −80 to −90 mV) and elevated [K+] Ringer's (most frequently, [K+] = 13 mM; estimated membrane potential, −60 to −65 mV). The frequency of sparks was 0.04–0.05 sarcomere−1 s−1 in normal Ringer's; the frequency increased approximately tenfold in 13 mM [K+] Ringer's. Spark properties in each solution were similar for the two species; they were also similar when scanned in the x and the y directions. From fits of standard functional forms to the temporal and spatial profiles of the sparks, the following mean values were estimated for the morphological parameters: rise time, ∼4 ms; peak amplitude, ∼1 ΔF/F (change in fluorescence divided by resting fluorescence); decay time constant, ∼5 ms; full duration at half maximum (FDHM), ∼6 ms; late offset, ∼0.01 ΔF/F; full width at half maximum (FWHM), ∼1.0 μm; mass (calculated as amplitude × 1.206 × FWHM3), 1.3–1.9 μm3. Although the rise time is similar to that measured previously in frog cut fibers (5–6 ms; 17–23°C), cut fiber sparks have a longer duration (FDHM, 9–15 ms), a wider extent (FWHM, 1.3–2.3 μm), and a strikingly larger mass (by 3–10-fold). Possible explanations for the increase in mass in cut fibers are a reduction in the Ca2+ buffering power of myoplasm in cut fibers and an increase in the flux of Ca2+ during release.


1990 ◽  
Vol 259 (2) ◽  
pp. E148-E154 ◽  
Author(s):  
H. S. Hundal ◽  
P. Babij ◽  
P. W. Watt ◽  
M. R. Ward ◽  
M. J. Rennie

Rat skeletal muscle glutamine fell by 40% from 4.18 to 2.5 mumols/g wet weight (P less than 0.01) after 4 days of denervation. Over the same period net glutamine efflux from denervated hindlimbs [i.e., arteriovenous (a-v) concentration differences x blood flow] increased 3.5-fold (from -6.72 +/- 1.73 to -26 +/- 4.81 nmol.min-1.g-1, P less than 0.001). Gastrocnemius glutamine synthetase activity fell 48% after denervation (from 475 +/- 81 to 248 +/- 39 nmol.min-1.g-1, P less than 0.001), but glutaminase activity was not significantly altered (17 nmol.min-1.g-1). The maximal activity (Vmax) of the unidirectional Na(+)-dependent glutamine transporter (system Nm) was depressed by 45% from 1,020 +/- 104 to 571 +/- 9 nmol.min-1.g-1 (P less than 0.01), but the concentration at which transport was half maximal (Km) was not significantly altered (control 8.1 +/- 0.6 mM; denervated 6.52 +/- 0.12). Hindlimb denervation resulted in an increase of intramuscular Na+ by 17% and a fall of K+ by 12%, and the resting membrane potential in isolated muscles decreased from -75 +/- 10 to -59.5 +/- 5.5 mV. Membrane potential of perfused denervated muscle, isolated after acute addition of the Na+ channel blocker tetrodotoxin (TTX, 3 microM), repolarized to -66.4 +/- 3.2 mV. In perfused denervated preparations TTX caused an acute recovery of Vmax of unidirectional glutamine transport to 848 +/- 75 nmol.min-1.g-1; Km was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)


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