The effect of ionophore A23178 on the α-actinin crosslinks in the z-band of frog skeletal muscle: An EM study

1986 ◽  
Vol 44 ◽  
pp. 154-155
Author(s):  
F.T. Llados ◽  
V. Krlho ◽  
G.D. Pappas
Keyword(s):  
Muscle Damage ◽  
Transmitter Release ◽  
Skeletal Muscles ◽  
Calcium Uptake ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Ach Release ◽  
Sustained Action ◽  
Calcium Deposits ◽  
Intense Stimulation

It Is known that Ca++ enters the muscle fiber at the junctional area during the action of the neurotransmitter, acetylcholine (ACh). Pappas and Rose demonstrated that following Intense stimulation, calcium deposits are found In the postsynaptic muscle membrane, Indicating the existence of calcium uptake In the postsynaptic area following ACh release. In addition to this calcium uptake, when mammal Ian skeletal muscles are exposed to a sustained action of the neurotransmitter, muscle damage develops. These same effects, l.e., Increased transmitter release, calcium uptake and finally muscle damage, can be obtained by Incubating the muscle with lonophore A23178.

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

Dual effects of opioids on transmitter release, intracellular calcium and calcium uptake in SK-N-SH cell line

1994 ◽  
Vol 54 (1) ◽  
pp. 253-254 ◽  
Author(s):  
Y Sarne ◽  
M Gafni ◽  
A Fields ◽  
O Keren
Keyword(s):  
Intracellular Calcium ◽  
Cell Line ◽  
Transmitter Release ◽  
Calcium Uptake

Membrane domain localization of pH-regulating transporters in frog skeletal muscle membrane vesicles

1996 ◽  
Vol 271 (4) ◽  
pp. C1367-C1379 ◽  
Author(s):  
R. W. Putnam ◽  
P. B. Douglas ◽  
N. A. Ritucci
Keyword(s):  
Skeletal Muscle ◽  
Atpase Activity ◽  
Surface Membrane ◽  
Membrane Vesicles ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Membrane Domain ◽  
Ph Response ◽  
Kinase C ◽  
Inside Out

The distribution of pH-regulating transporters in surface and transverse (T) tubular membrane (TTM) domains of frog skeletal muscle was studied. 2',7'-Bis(carboxyethyl)-5(6)- carboxyfluorescein-loaded giant sarcolemmal vesicles, containing surface membrane, exhibited reversible Na+/H+ exchange. A microsomal vesicle fraction was shown to be enriched in TTM on the basis of high Na(+)-K(+)-ATPase and Mg(2+)-ATPase activity, high ouabain and nitrendipine binding, and low Ca(2+)-ATPase activity. TTM vesicles were well sealed and oriented inside out. Vesicles were loaded with the pH-sensitive dye pyranine. In response to an inwardly directed Na+ gradient, vesicles displayed virtually no alkalinization unless monensin was present. No pH response to an imposed Na+ gradient was seen regardless of the direction of the pH gradient across the vesicles, after phosphorylation of the vesicles with protein kinase C, or when exposed to guanosine 5'-O-(3-thiotriphosphate). In the presence of CO2, addition of Na+ or Cl- had no effect on vesicle pH. These data indicate that the TTM lacks functional pH-regulating transporters [Na+/H+ and (Na+ + HCO3-)/Cl- exchangers], suggesting that pH-regulating transporters are localized only to the surface membrane domain in frog muscle.

Can Estrogens Diminish Exercise Induced Muscle Damage?

1995 ◽  
Vol 20 (1) ◽  
pp. 26-38 ◽  
Author(s):  
Peter M. Tiidus
Keyword(s):  
Free Radical ◽  
Muscle Damage ◽  
Membrane Lipids ◽  
Female Rats ◽  
Male Rats ◽  
Muscle Membrane ◽  
Potential Significance ◽  
Membrane Stabilization ◽  
Female Sex Hormones ◽  
Exercise Induced

Estrogens are female sex hormones that may also protect against peroxidative damage of membrane lipids and low density lipoproteins (LDL). Studies have reported that female rats have greater protection against free radical induced lipid peroxidation and muscle damage consequent to exercise than do male rats. It has been suggested that the lower susceptibility to exercise induced oxidative stress and muscle membrane disruption of female rats may be due primarily to the antioxidant and membrane stabilizing properties of estrogens. Studies on humans have indicated that the lower incidence of atherosclerosis seen in premenopausal females in comparison to males is due at least in part to the ability of estrogens to diminish LDL peroxidation. However, there is little evidence as to the potential of estrogens to protect human females from free radical induced peroxidation and muscle damage due to exercise. This paper reviews the evidence for membrane stabilization potential of estrogens and their possible mechanisms, and speculates as to the potential significance of this for human exercise. Key words: estradiol, atherosclerosis, free radicals, peroxidation, antioxidants

scholarly journals Synaptic excitation is regulated by the postsynaptic dSK channel at the Drosophila larval NMJ

2014 ◽  
Vol 111 (12) ◽  
pp. 2533-2543 ◽  
Author(s):  
Daniel M. Gertner ◽  
Sunil Desai ◽  
Gregory A. Lnenicka
Keyword(s):  
Transmitter Release ◽  
Membrane Conductance ◽  
Postsynaptic Membrane ◽  
Synaptic Activity ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Excitation ◽  
Sk Channel ◽  
Larval Neuromuscular Junction

In the mammalian central nervous system, the postsynaptic small-conductance Ca2+-dependent K+ (SK) channel has been shown to reduce postsynaptic depolarization and limit Ca2+ influx through N-methyl-d-aspartate receptors. To examine further the role of the postsynaptic SK channel in synaptic transmission, we studied its action at the Drosophila larval neuromuscular junction (NMJ). Repetitive synaptic stimulation produced an increase in postsynaptic membrane conductance leading to depression of excitatory postsynaptic potential amplitude and hyperpolarization of the resting membrane potential (RMP). This reduction in synaptic excitation was due to the postsynaptic Drosophila SK (dSK) channel; synaptic depression, increased membrane conductance and RMP hyperpolarization were reduced in dSK mutants or after expressing a Ca2+ buffer in the muscle. Ca2+ entering at the postsynaptic membrane was sufficient to activate dSK channels based upon studies in which the muscle membrane was voltage clamped to prevent opening voltage-dependent Ca2+ channels. Increasing external Ca2+ produced an increase in resting membrane conductance and RMP that was not seen in dSK mutants or after adding the glutamate-receptor blocker philanthotoxin. Thus it appeared that dSK channels were also activated by spontaneous transmitter release and played a role in setting membrane conductance and RMP. In mammals, dephosphorylation by protein phosphatase 2A (PP2A) increased the Ca2+ sensitivity of the SK channel; PP2A appeared to increase the sensitivity of the dSK channel since PP2A inhibitors reduced activation of the dSK channel by evoked synaptic activity or increased external Ca2+. It is proposed that spontaneous and evoked transmitter release activate the postsynaptic dSK channel to limit synaptic excitation and stabilize synapses.

The Effect of Sodium and Potassium on Calcium Uptake by Frog Skeletal Muscle Mitochondria and Vesicles

1972 ◽  
Vol 50 (12) ◽  
pp. 1157-1161 ◽  
Author(s):  
Satish Batra
Keyword(s):  
Skeletal Muscle ◽  
Calcium Uptake ◽  
Frog Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Sucrose Medium ◽  
Ca Uptake ◽  
Sodium And Potassium

Calcium uptake by mitochondria of frog skeletal muscle increased when K replaced Na or sucrose in the medium. There was no difference in passive binding of Ca and the amount of ATP split when K replaced Na. Ca uptake was increased by substituting K for Na in the medium and was maximal in a medium containing 100 mM K and no Na. Azide and dinitrophenol (DNP) inhibited K-stimulated Ca uptake completely. Inhibition by these agents in Na medium was relatively small. Ca uptake by vesicles was little affected by changing from Na to K medium, by azide, or by DNP. Ageing reduced Ca uptake in both fractions and stimulation by K of mitochondrial Ca uptake nearly disappeared after 4 h of storage (at 4 °C). Since Ca was taken up to the same extent in Na or sucrose medium, it is concluded that Ca uptake by mitochondria is stimulated by K rather than inhibited by Na.

Muscle Damage After Delivery of Naked Plasmid DNA into Skeletal Muscles Is Batch Dependent

2011 ◽  
Vol 22 (2) ◽  
pp. 225-235 ◽  
Author(s):  
Christine I. Wooddell ◽  
Vladimir M. Subbotin ◽  
Magdolna G. Sebestyén ◽  
Jacob B. Griffin ◽  
Guofeng Zhang ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Plasmid Dna ◽  
Skeletal Muscles ◽  
Naked Plasmid ◽  
Naked Plasmid Dna

scholarly journals Intracellular Calcium Movements of Frog Skeletal Muscle during Recovery from Tetanus

1968 ◽  
Vol 51 (1) ◽  
pp. 65-83 ◽  
Author(s):  
Saul Winegrad
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Skeletal Muscles ◽  
Room Temperature ◽  
Complete Recovery ◽  
Mechanical Activity ◽  
Tetanic Stimulation ◽  
Frog Skeletal Muscle ◽  
Fixation Techniques ◽  
Terminal Cisternae

Radioautographs of 45Ca-labeled frog skeletal muscles have been prepared using freeze-dry and vapor fixation techniques to avoid displacement of the isotope during the preparation of the radioautographs. 45Ca has been localized in resting muscles exposed to 45Ca Ringer's for 5 min or 5 hr and in isotopically labeled muscles recovering from tetanic stimulation at room temperature or at 4°C. In muscles soaked at rest for 5 min 45Ca was present almost exclusively in the terminal cisternae. In all other muscles there were three sites at which the isotope was concentrated: (a) the terminal cisternae, (b) the intermediate cisternae and the longitudinal tubules, and (c) the A band portion of the myofibrils. The terminal cisternae were labeled more rapidly than the myofibrils, but both exchanges were accelerated by electrical stimulation. The amount of 45Ca in the longitudinal tubules and the intermediate cisternae decreased with time after a tetanus as the amount in the terminal cisternae increased. It is proposed that electrical stimulation releases calcium from the terminal cisternae and that relaxation occurs from the binding of the released calcium by the longitudinal tubules and the intermediate cisternae. Complete recovery from mechanical activity involves the transport of this bound calcium into the reticulum and its subsequent binding by the terminal cisternae. Resting exchange of calcium occurs primarily between the terminal cisternae and the transverse tubules.

Sign in / Sign up

Export Citation Format

Share Document