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PubMed1989

Innervation of regenerated spindles in muscle grafts of the rat.

Features of the nerve supply and the encapsulated fibers of muscle spindles were assessed in grafted and normal extensor digitorum longus (EDL) muscles of rats by analysis of serial 10-microns frozen transverse sections stained for enzymes which delineated motor and sensory endings, oxidative capacity and muscle fiber type. The number of fibers was significantly more variable, and branched fibers were more frequently observed in regenerated spindles than in control spindles. Forty-eight percent of regenerated spindles received sensory innervation. Spindles reinnervated by afferents had a larger periaxial space than did spindles which were not reinnervated by afferents. Regenerated fibers innervated by afferents had small cross-sectional areas, equatorial regions with myofibrils restricted to the periphery of fibers, unpredictable patterns of nonuniform and nonreversible staining along the length of the fiber for 'myofibrillar' adenosine triphosphatase (mATPase) after acid and alkaline preincubation. In contrast, regenerated fibers devoid of sensory innervation resembled extrafusal fibers in that they usually exhibited myofibrils throughout the length of the fiber, no central aggregations of myonuclei, uniform staining for mATPase and a reversal of staining for mATPase after preincubation in an acid or alkaline medium. Approximately thirty percent of encapsulated fibers devoid of sensory innervation stained analogous to a type I extrafusal fiber, a pattern of staining never observed in intrafusal fibers of normal spindles. Groups of encapsulated fibers all exhibiting this pattern of staining reflect that either these fibers may have been innervated by collaterals of skeletomotor axons that originally innervated type I extrafusal fibers or that fibers innervated by only fusimotor neurons express patterns of staining for mATPase similar to extrafusal fibers in the absence of sensory innervation. Sensory innervation may also influence the reestablishment of multiple sites of motor endings on regenerated intrafusal fibers. Those regenerated fibers innervated by afferents had more motor endings than did regenerated fibers devoid of sensory innervation. Differences in size, morphology, and patterns of staining for mATPase and numbers of motor endings between fibers innervated by afferents and fibers devoid of sensory innervation reflect that afferents can influence the differentiation of muscle cells and the reestablishment of motor innervation other than during the late prenatal/early postnatal period when muscle spindles form and differentiate in rats.

Adenosine Triphosphatases↗

PubMed1980

A quantitative estimation of components in crayfish muscle fibres by stereological methods.

The volume and surface densities of structural components in isolated long-sarcomere fibres of crayfish (Astacus fluviatilis) were estimated by stereological methods. The relative volumes were as follows (in % of the fibre volume): sarcolemmal invaginations (SI) 0.74; T-system 1.1; whole sarcoplasmic reticulum (SR) 4.7; junctional SR cisternae 0.41; mitochondria 1.1; nuclei 0.57; myofibrils 81.6; peripheral basal lamina 1.1; junctional gap 0.043; lysosomes 0.029. The values for surface densities were (in microns2/100 microns3): peripheral sarcolemma 1.27; SI 7.21; T-system 40.2; whole SR 146.4; junctional SR cisternae 14.88; junctional area of SR cisternae 7.05; mitochondria 8.98; nuclei 0.75; myofibrils 163. The invaginated membranes (SI and T-system) made up 97.4% of the total area of surface membranes and increased the effective area of peripheral sarcolemma 39 times. Using the values of the total electrical capacity from previous investigations on Astacus fibres, the specific capacity of surface membranes was calculated as 1.08 microF/cm2.

Animals↗

PubMed1980

Ca2+ and Sr2+ activation: comparison of cardiac and skeletal muscle contraction models.

The mechanism of contraction in rabbit fast-twich, and bovine and rabbit cardiac muscle was examined using functionally skinned fibers, ATPase activity of myofibrils, and cardiac or skeletal troponin-tropomyosin regulated actin heavy meromyosin. The Ca2+ and Sr2+ activation properties for the different measures of contraction were evaluated. (1) Tension in rabbit and bovine cardiac skinned fibers and rabbit cardiac myofibrillar ATPase were activated equally well by either Ca2+ or Sr2+. By contrast, rabbit adductor magnus (fast-twich) skinned fibers required substantially higher [Sr2+] than [Ca2+] for activation, as did rabbit myofibrils from back muscle (fast-twitch). (2) Substantially more Sr2+ than Ca2+ was also required for activation of skeletal muscle actin heavy meromyosin ATPase, controlled by either the skeletal or cardiac troponin-tropomyosin complex, similar to the activation of fast-twitch muscle. (3) The absence of correlation between the divalent cation selectivity properties of actin heavy meromyosin ATPase controlled by cardiac troponin-tropomyosin and cardiac muscle tension or myofibrillar ATPase activation by Ca2+ and Sr2+ suggests that troponin, if primarily responsible for the activation of cardiac muscle, has very different in vivo and in vitro binding properties. (4) The close correlation between percentage of maximal Ca2+- and Sr2+-activated myofibrillar ATPase and tension in skinned fibers strongly justifies the use of myofibrillar ATPase, in contrast to a reconstituted troponin-tropomyosin actin heavy meromyosin ATPase system, as a biochemical measure of contraction.

Adenosine Triphosphatases↗

PubMed1988

Skeletal muscle pathology in ovine congenital progressive muscular dystrophy. 1. Histopathology and histochemistry.

The histopathological lesions of ovine congenital progressive muscular dystrophy (CPMD) were characterized by myofiber hypertrophy, focal myofibrillar degeneration, formation of peripheral and central sarcoplasmic masses devoid of myofibrils and internal nuclei often in chains. Progressive loss of myofibrils was associated with atrophy of the fiber and eventual collapse of the sarcolemma. The process was polyphasic, consequently in mature lesions there was great variation in fiber diameter. Split fibers were common but ring fibers occurred rarely. Myofiber loss was associated with fatty or fibrous tissue replacement. Only type I (red, slow twitch, oxidative) fibers were affected and there was no histological evidence of effective regeneration. Ovine CPMD has many histopathological features in common with dystrophia myotonica in humans.

Adenosine Triphosphatases↗

PubMed1980

Localization of arginine kinase in muscles fibres of Drosophila melanogaster.

Arginine kinase (AK), a monomeric protein of mol. wt. 40 000, was purified from adult Drosophila melanogaster. Antiserum to AK was raised in rabbits; its specificity was established by immunodiffusion tests and by immunoreplicas of electropherograms. After electrophoresis in non-denaturing conditions, the immunoreactive material was shown to possess enzymatic activity. Localization of AK by indirect immunofluorescence on washed myofibrils showed that at least a fraction of the total cellular AK is bound to the contractile apparatus. In muscle fibres of third instar larvae and in isolated adult fibrillar flight muscle myofibrils, AK was localized within the Z-line region. Adult tubular muscle fibres (tergal depressor of the trochanter) showed fluorescence in the A-band. In all cases, the localization was independent of the state of contraction. Vertebrate B- and M-type creatine kinases have previously been localized at the Z-line and A-band (M-line) regions, respectively. Isoenzymic forms of AK have not been detected in Drosophila, however.

Animals↗

PubMed1982

Quantification of tropomyosin by radioimmunoassay in developing hearts of cardiac mutant axolotls, Ambystoma mexicanum.

Recessive mutant gene c in axolotls results in a failure of embryonic heart function. Earlier morphological studies showed that the mutant myocardial cells lack organized sarcomeric myofibrils. Electrophoresis and immunofluorescent studies suggested that the mutant heart cells contain substantial amounts of actin, myosin and alpha-actinin; however, tropomyosin appeared deficient. In the present study, we employed a newly developed extremely sensitive solid-phase radioimmunoassay method to quantitate very accurately the tropomyosin levels in normal and mutant sibling hearts at early (stage 35), intermediate (stage 39) and late (stage 41) developmental stages. Our results demonstrate that cardiac mutant hearts contain significantly lower than normal quantities of antigenically detectable tropomyosin at all of the developmental stages examined. This insufficiency of tropomyosin in mutant hearts may be a primary cause at the cell level for their failure to form organized myofibrils.

Ambystoma↗

PubMed1983

Isoenzyme-specific localization of M-line bound creatine kinase in myogenic cells.

Experiments using isolated fibre bundles or myofibrils of chicken skeletal muscle have shown that a relatively small portion of the muscle-specific MM-type of creatine kinase (CK) (EC 2.7.3.2) is specifically bound to the M-line and yet greatly contributes to the electron-dense M-line structure. Here we demonstrate the presence of M-line bound CK in cultured myogenic cells by removing the unbound sarcoplasmic CK through permeabilization with Triton X-100 and extensive washing of the cells prior to immunofluorescence staining. When stained with antibodies specific for M-CK subunits these cells exhibit bright fluorescence within the M-line region of myofibrils. Occasionally this cross-striated pattern is also observed in mononucleated presumably postmitotic myoblasts. Anti-B-CK incubation, in contrast, results in a weak, diffuse fluorescence at the Z-band. Even though these cells contain appreciable amounts of B-type CK, specific fluorescence at the M-line is never observed with anti-B-CK antibody thus ruling out the presence of BB-type or MB-type CK at this location. Therefore the presence of CK within the M-line structure of myogenic cells which contain all three CK isoenzymes seems to be restricted to the MM-type isoenzyme.

Animals↗

PubMed1997

Ca(2+)-dependent and Ca(2+)-independent regulation of contractility in isolated human myocardium.

UNLABELLED: Changes in contractile force of the myocardium may depend on changes in the intracellular Ca2+ concentration, changes in the responsiveness of the myofibrils for Ca2+, or a combination of both. We investigated in isolated muscle strip preparations from human nonfailing and endstage failing hearts the influence of physical (changes in preload, stimulation rate, or rhythm), and pharmacological interventions (alpha- or beta-adrenoceptor-stimulation, endothelin) on developed force of contraction and the corresponding intracellular Ca2+ transients. METHODS: Isometric contraction, electrical stimulation, 37 degrees C. Simultaneous registration of force of contraction and intracellular Ca2+ transients (aequorin method). RESULTS: Increases in preload, alpha- and endothelin-receptor stimulation resulted in increases in force of contraction without increasing aequorin light emission. Increasing stimulation rate or increasing rest intervals resulted in parallel increases (nonfailing myocardium) or decreases (failing myocardium) of force of contraction and aequorin light emission. beta-Adrenoceptor-stimulation exerted inotropic and lusitropic effects in human failing myocardium associated with a large, overproportional increase in aequorin light emission. CONCLUSION: The human heart regulates intrinsic contractility via several subcellular mechanisms. Increases in preload (Frank-Starling-mechanism) and alpha- or endothelin-receptor-stimulation enhance myocardial contractility by increasing the Ca2+ responsiveness of the myofilaments; rate- and rhythm-dependent modulation of the contractile state directly depend on changes in the intracellular Ca(2+)-transients; beta-adrenoceptor stimulation results in an overproportional large increase in intracellular Ca2+ transients, probably due to additional cAMP-dependent Ca(2+)-desensitizing effects on the level of the myofibrils.

Calcium↗

PubMed1994

Role of regulatory proteins (troponin-tropomyosin) in pathologic states.

In vertebrate striated muscle, troponin-tropomyosin is responsible, in part, not only for transducing the effect of calcium on contractile protein activation, but also for inhibiting actin and myosin interaction when calcium is absent. The regulatory troponin (Tn) complex displays several molecular and calcium binding variations in cardiac muscles of different species and undergoes genetic changes with development and in various pathologic states. Extensive reviews on the role of tropomyosin (Tm) and Tn in the regulation of striated muscle contraction have been published describing the molecular mechanisms involved in contractile protein regulation. In our studies, we have found an increase in Mg2+ ATPase activity in cardiac myofibrils from dystrophic hamsters and in rats with chronic coronary artery narrowing. The abnormalities in myofibrillar ATPase activity from cardiomyopathic hamsters were largely corrected by recombining the preparations with a TnTm complex isolated from normal hamsters indicating that the TnTm may play a major role in altered myocardial function. We have also observed down regulation of Ca2+ Mg2+ ATPase of myofibrils from hypertrophic guinea pig hearts, myocardial infarcted rats and diabetic-hypertensive rat hearts. In myosin from diabetic rats, this abnormality was substantially corrected by adding troponin-tropomyosin complex from control hearts. All of these disease models are associated with decreased ATPase activities of pure myosin and in the case of rat and hamster models, shifts of myosin heavy chain from alpha to beta predominate. In summary, there are three main troponin subunit components which might alter myofibrillar function however, very few direct links of molecular alterations in the regulatory proteins to physiologic and pathologic function have been demonstrated so far.

Actins↗

PubMed1978

The larval electric organ of the weakly electric fish Pollimyrus (Marcusenius) isidori (Mormyridae, Teleostei).

The larval electric organ of Pollimyrus isidori consists of four longitudinal tubes, a dorsal and a ventral pair, which begin behind the skull, end at the beginning of the caudal peduncle and show myotomic segmentation. The elementary units are, apparently, transformed muscle fibres called electrocytes. They are shorter and thicker than muscle fibres, with long stalks and are found in the medial part of the deep lateral muscle. Electron microscopy reveals a clear difference between the anterior and posterior face of the electrocyte. Anteriorly, deep linear invaginations of the surface membrane together with many small vesicles of about 100 nm diameter can be seen. Posteriorly, many plasma membrane invaginations and vacuoles are found together with numerous cytoplasmic organelles--pleiomorphic nuclei, Golgi apparatus, oblong mitochondria and multivesicular bodies. The stalk originates at the posterior face and the nerve terminals are situated at the distal end of the stalk. In the electrocyte, myofibrils, similar to those found in muscle fibres, can be detected with clearly visible Z lines but with only a suggestion of H zones. Two bundles of myofibrils can be seen arranged orthogonally in the electrocyte. Strong acetylcholinesterase activity was found on the anterior face and on the innervated stalk. Under the given recording conditions the overall discharge amplitude of the larval electric organ reaches a maximum of about 100 mV peak to peak. The pulse duration is 1 millisecond and the main phase is head-positive.

Animals↗

PubMed1990

Unexpected infant death attributable to cardiac tumor or cardiomyopathy. Immunohistochemical and electron microscopical findings in three cases.

The pathological findings, including immunohistochemical and electron microscopical findings, in three infants who died unexpectedly of cardiac tumor or cardiomyopathy are reported. The first was a 13-month-old boy with tuberous sclerosis and multiple rhabdomyomas of the heart, who presented with a postpartal cardiac murmur and moderate cardiomegaly. The further history was unknown. The rhabdomyoma nodules were composed of spider cells containing small amounts of desmin and myosin as well as isolated myofibrils. Microscopically small glioma nodules contained high amounts of GFAP. The second case, a boy 4 months of age, died of a large benign fibrous histiocytoma of the heart after an uneventful history. Tumor cells contained alpha-1-anti-chymotrypsin and lysozyme. The third case, a girl 2 months of age, died unexpectedly of histiocytoid cardiomyopathy. The affected cells contained fat droplets, glycogen granules, many leptomer myofibrils and small amounts of myosin and desmin.

Astrocytoma↗

PubMed1993

Muscle regeneration after exercise-induced myoglobinuria: an electron microscopic study.

Muscle regeneration was studied by light and electron microscopy in a case of exercise-induced acute myoglobinuria in a young patient with carnitine-palmityl-transferase deficiency. Various stages of regeneration existed in the foci of necrosis scattered throughout apparently normal muscle. Activated satellite cells, myoblasts and myotubes were found, some of them containing myofibrils. Among the cells accumulating in the necrotic fibres, some apparently contained surviving myonuclei. In some fibres of normal size, developing myofibrils were abundant. Surviving myonuclei may be of significance in the reaction of muscle cells after injury.

Child, Preschool↗

PubMed1991

Diethylene glycol (DEG)-associated myocardial changes: a pilot investigation of chronic intoxication in guinea-pigs.

The myocardium of guinea pigs fed on sublethal doses of diethylene glycol (DEG) over a period of 2-11 days was examined for microscopical and ultrastructural changes. Coagulative myocytolysis and loss of myofibrils, not observed in the controls, was patchily distributed throughout the myocardium. The accompanying ultrastructural features included swelling, pleomorphism and hyperplasia of mitochondria with an associated distension of the interfibrillary spaces and a displacement, distortion and rupture of adjacent myofibrils.

Administration, Oral↗

PubMed1992

In situ compartmentation of creatine kinase in intact sarcomeric muscle: the acto-myosin overlap zone as a molecular sieve.

Creatine kinase isoenzymes (CK = ATP: creatine N-phosphoryl transferase, EC 2.7.3.2) were localized in situ in cryosections of intact sarcomeric muscle by immunocytochemical staining. Similar to cardiac muscle, spermatozoa and photoreceptor cells, mitochondrial-type CK (Mi-CK) localization in skeletal muscle was also restricted to mitochondria. Besides the well-documented localization of muscle-type (M-CK) at the M-line and at the sarcoplasmic reticulum, surprisingly, most of the sarcoplasmic M-CK was also highly compartmentalized and was mainly confined to the I-band. The localization of M-CK at the I-band coincided with that of adenylate kinase and aldolase. In intact muscle, the diffusion equilibrium decisively favours occupancy by all three enzymes of the I-band, with the acto-myosin overlap region of the A-band acting as a molecular sieve, excluding to a large extent all three enzymes from the acto-myosin overlap region. This indicates that in intact muscle, this region of the A-band may be less accessible in vivo to soluble, sarcoplasmic enzymes than thought before. If muscle were permeabilized by chemical skinning before fixation, I-band CK, as well as aldolase and adenylate kinase, were solubilized and disappeared from the myofibrils, but the fraction of M-CK which was specifically associated with the M-line remained bound to the myofibrils. Implications of these findings are discussed with respect to the functional coupling of I-band-CK with glycolysis, to the formation of large multienzyme complexes of glycolytic enzymes with CK and to the supply of energy for muscle contraction in general.

Actins↗

PubMed1989

Ultrastructural localization of calcium in post-mortem bovine muscle: a cytochemical and X-ray microanalytical study.

Calcium localization was demonstrated in bovine longissimus muscle using the antimonate precipitation technique in combination with electron probe X-ray microanalysis. Samples were taken each hour during the first 24 h post-mortem, and then after a storage period of 8 and 15 days. For all sampling times analysed, heavy precipitates were seen in dense parts of nuclei and on N-lines of myofibrils. Up to 18-20 h post-mortem, deposits were observed in sarcoplasmic reticulum at the level of triads. In comparison with the earlier post-mortem samples, myoplasmic precipitates were strongly increased at 4 h post-mortem, and just before rigor onset, at 19 h where intermyofibrillar spaces were completely blackened and triads were no more visible. These localizations of precipitates were still observed up to 15 days post-mortem. At these storage times, myofibril disruptions were seen at the level of N-lines. Wavelength-dispersive and energy-dispersive spectrometric analyses indicated that significant amounts of calcium occurred in the dense precipitates observed.

Animals↗

PubMed1989

Regulation of force and intracellular calcium transients by cyclic AMP generated by forskolin, MDL 17,043 and isoprenaline, and its modulation by muscarinic receptor agents: a novel mechanism for accentuated antagonism.

The relation of changes in intracellular calcium transients and force of isometric contractions in response to an elevation or reduction of cyclic AMP levels was investigated in isolated dog ventricular trabeculae and rabbit papillary muscles, in which multiple superficial cells have been microinjected with the calcium sensitive bioluminescent protein aequorin. Forskolin, MDL 17,043 and isoprenaline elevated the tissue cyclic AMP level, increased consistently the peak aequorin signals and force, and abbreviated the duration of both signals in a concentration-dependent manner. When the effect of isoprenaline was compared with that of alteration of extracellular calcium concentration [( Ca2+]0), the increase in force by isoprenaline was associated with higher peak aequorin signals than that by alteration of [Ca2+]0 for a given increase in force, indicating the decrease in calcium sensitivity of myofibrils by cyclic AMP generated by beta-adrenoceptor stimulation. Carbachol, which did not affect significantly the basal force and cyclic AMP levels, lowered the cyclic AMP levels elevated previously by forskolin, MDL 17,043 or isoprenaline in the isolated dog ventricular trabeculae. It antagonized the increase in peak aequorin signals and force caused by these agents in a concentration-dependent manner. When carbachol had been administered prior to isoprenaline and the concentration-response curve for isoprenaline was determined in the presence of carbachol, the relation of force peak aequorin signals was not modified by carbachol in the rabbit papillary muscle. Carbachol, when administered during induction of the positive inotropic action by forskolin, MDL 17,043 and isoprenaline, decreased the force more than peak aequorin signals in a concentration-dependent manner in the dog ventricular trabeculae. Therefore, the relation of force to peak aequorin signals was shifted downwards during the carbachol-induced inhibition, indicating a further decrease of calcium sensitivity of myofibrils by carbachol. This effect of carbachol appears to be specific to the cyclic AMP-mediated positive inotropic action, since the alpha-adrenoceptor-mediated (cyclic AMP-independent) action was unaffected by carbachol. This mechanism may play an important role for "accentuated antagonism" in the mammalian ventricular myocardium.

Animals↗

PubMedDate not supplied

Comparative aspects of cardiac ultrastructure, morphometry, and electrocardiography of hearts from rats fed restricted dietary copper and selenium.

Comparative cardiac ultrastructure, morphometry, and electrocardiography after dietary copper and selenium restriction were examined. Male weanling Long-Evans rats were fed diets that were either adequate in both copper and selenium (Cu+/Se+) or restricted in either Cu (Cu-) or Se (Se-) for 8 wk. At wk 8, electrocardiograms (ECG) and dP/dts were obtained and heart tissue was utilized for electron microscopy. Upon examination, Cu- rats were anemic, exhibited a greater heart: body weight ratio, and developed concentric hypertrophy characterized by an enhanced thickening of the left and right ventricular free walls, and interventricular septum. ECG recordings from lead aVF in the Cu- group showed a greater R wave amplitude in comparison to the Cu+/Se+ group. Se- rats recorded a greater left ventricular +dP/dtmax than both the Cu+/Se+ and Cu- groups. Cardiac myofibril volume densities were decreased in both Cu- and Se- rats in comparison to the Cu+/Se+ rats. In addition Cu- rats showed a greater mitochondria:myofibril ratio. Sarcomere contractile protein disarray was present in both the Cu- and Se- groups. Se- myocytes also showed evidence of edema and mitochondrial fragmentation. The subcellular alterations suggest that similarities exist in the cardiac remodeling processes associated with copper and selenium restrictions.

Animals↗

PubMed2001

Plasticity of myosin heavy chain expression with temperature acclimation is gradually acquired during ontogeny in the common carp (Cyprinus carpio L.).

Common carp (Cyprinus carpio L.) were reared from hatching until 61 mm total length (TL) at 21 degrees C. At 14 weeks and 20 weeks post-hatch, corresponding to initial lengths of 30 mm and 44 mm respectively, fish were acclimated to 10 degrees C using a rate of cooling of 1 degrees C per day. A statistical model was used to compare the time course in the change of white muscle myofibrillar ATPase activity with temperature acclimation. The myosin heavy chain (MHC) composition of white muscle myofibrils was investigated using peptide mapping. A significant increase in myofibrillar ATPase activity was observed after 2-3 weeks in the 44 mm group, but not until 4-5 weeks in the 30 mm group. when they had reached 37 mm TL. The MHC banding pattern of 120 mm TL fish acclimated to 10 degrees C or 21 degrees C for a minimum of 6 weeks were distinct from each other. The MHC peptide map characteristic of 10-degrees C-acclimated fish was not observed in individuals less than 37 mm length. We therefore conclude that the capacity to alter the composition and properties of myofibrils with cold acclimation is acquired in juvenile carp at around 37 mm TL.

Acclimatization↗