Sustained GABA-induced regulation of the L -type Ca 2+ conductance in crustacean muscle fibers

1997 ◽  
Vol 434 (3) ◽  
pp. 272-279 ◽  
Author(s):  
Juan Castellote ◽  
Alfonso Araque ◽  
W. Buño
1978 ◽  
Vol 77 (1) ◽  
pp. 48-58 ◽  
Author(s):  
AB Eastwood ◽  
DS Wood ◽  
JP Reuben

The proximal accessory flexor (PAF) of the myochordotonal organ (MCO) in the meropodite of crayfish walking legs contains two populations of muscle fibers which are distinguishable by their diameters. The large accessory (LA) fibers are 40-80 micrometer in diam and are similar in ultrastructure to other slow crustacean fibers. The small accessory (SA) fibers are 1-12 micrometer in diam and have a unique myofilament distribution at normal body lengths. There is extensive double overlap of thin filaments at these lengths, and some of them form bundles that may extend the length of the sarcomere. In the middle of the sarcomeres, thick and thin filaments are totally segregated from each other. When the fibers are stretched to lengths beyond double overlap length, the myofilament patterns are conventional. The segregated pattern is reestablished when stretched fibers are allowed to shorten passively. The length-tension relationship of the SA fibers is described by a linear ascending branch, a plateau, and a linear descending branch. The ascending branch encompasses normal body lengths from slack length (Ls) with maximum double overlap to the length at which double overlap ceases (1.8 X Ls). The descending phase is comparable to that of other skeletal muscles. That is, tension decreases in proportion with the reduction in thick-thin filament interdigitation (2 X Ls to 3 X Ls).


1987 ◽  
Vol 65 (4) ◽  
pp. 672-680 ◽  
Author(s):  
Eduardo Rojas ◽  
Verónica Nassar-Gentina ◽  
Mario Luxoro ◽  
Michael E. Pollard ◽  
M. Angélica Carrasco

Intracellular applications of a fixed amount (0.2 to 8 nmol) of inositol 1,4,5-trisphosphate (InsP3) over a brief period (2 s) into barnacle muscle fibers induced vigorous contractures. Peak tension attained during the first application depended on [InsP3]; the maximum tension evoked by the injection of 8 nmol was 1.6 kg/cm2. Peak tension during a second application of a high dose of InsP3 (> 10 μM) was always smaller than that during the first application. Extracellular Ca2+ could be omitted with no measurable effects on either the amplitude or time course of the contractures evoked by InsP3. Aequorin was used to measure InsP3-evoked Ca2+ release from intracellular stores in minced muscle fibers from lobster and in skinned muscle fibers from barnacle. Provided the sarcoplasmic reticulum was preloaded with Ca2+, application of InsP3 induced a transient Ca2+ release that was [InsP3] dependent. During each transient, [Ca2+] rose rapidly to a peak value (t1/2 < 5 s) and then slowly returned (t1/2 < 100 s) to a basal level. Maximum Ca2+ release was obtained at [InsP3] < 100 μM and amounted to 4 nmol Ca2+/g of muscle, enough to increase [Ca2+]i from 0.1 to 8 μM had the Ca2+ release occurred in the intact fiber. Successive applications of a fixed amount of InsP3 elicited successive transient increases in Ca2+. The effects of [Ca2+] on the incorporation of [3H]inositol into the pools of phosphatidylinositol, phosphatidylinositol 4-phosphate, and phosphatidylinositol 4,5-bisphosphate pools were measured. At 1 μM [Ca2+] the levels of the labelled phosphoinositides increased from 0.98, 0.40, and 0.17 pmol/μmol phosphorus (measured at 0.1 μM) to 1.63, 0.54, and 0.46 pmol/μmol lipid phosphorus, for phosphatidylinositol, phosphatidylinositol 4-phosphate, and phosphatidylinositol 4,5-biphosphate, respectively. These data support the hypothesis that InsP3 could be an intracellular messenger, presumably between the site of Ca2+ entry at the level of the transverse tubular membrane and the sarcoplasmic reticulum membrane, which causes Ca2+ release from Ca2+-loaded sarcoplasmic reticulum in crustacean muscle.


Author(s):  
F. G. Zaki

Choline-deficiency was induced in Holtzman young rats of both sexes by feeding them a high fat - low protein diet.Preliminary studies of the ultrastructural changes in the myocardium of these animals have been recently reported from this laboratory. Myocardial lesions first appeared in the form of intraventricular mural thrombi, loss of cross striation of muscle fibers and focal necrosis of muscle cells associated with interstitial myocarditis. Prolonged choline-deficiency induced cardiomegaly associated with pericardial edema.During the early phase of this nutritional disorder, heart mitochondria - despite of not showing any swelling similar to that usually encountered in liver mitochondria of the same animal - ware the most ubiquitous site of marked structural abnormalities. Early changes in mitochondria appeared as vacuolation, disorganization, disruption and loss of cristae. Degenerating mitochondria were often seen quite enlarged and their matrix was replaced by whorls of myelin figures resembling lysosomal structures especially where muscle fibers were undergoing necrosis. In some areas, mitochondria appeared to be unusually clumped together where some contained membranelined vacuoles and others enclosed dense bodies and granular inclusions.


Sign in / Sign up

Export Citation Format

Share Document