Changes in leaching properties of chick skeletal muscles on denervation

The leaching of electrolytes in normal and denervated chick gastrocnemius muscle has been studied by recording electroconductivity changes in donor-solvent (muscle-water) system at 11 intervals leading to a total immersion of 5 hr 15 min, at days 1,5,10,21 and 28, post-hatching. The results show age related changes in the permeability properties of normal muscle membrane system. The loss of neural control induces a blocking of electrolytes 10 days post-denervation. The possible nature of blocking mechanism has been related to the non-availability of neuro-trophic factors in the tissue.     

Changes in lipid levels of three skeletal muscles following denervation

Nonpolar and polar lipids extracted from denervated rat gastrocnemius, plantaris, and soleus muscles were measured 7–9 days after unilateral sciatic nerve transection. The contralateral muscle (CCON) was used to obtain control lipid levels. After denervation changes in lipid concentrations were found in all three muscles. These alterations in lipid levels were generally in the same direction but not to the same extent. The change in total nonpolar lipids (NL) was an increase in soleus > gastrocnemius > plantaris concentration. This change in lipid concentration was more apparent than real since the wet weight of muscle was decreased after denervation. Since polar lipid (PL) concentrations were not increased under these conditions of muscle weight loss, an actual decrease of polar lipids after denervation may be inferred.In contrast to the other two muscles, a marked difference was noted for polar lipids of denervated gastrocnemius muscle. An unidentified spot near the origin was detected. This area is the location of a nerve sprouting factor(s). The compound(s) was not detectable for the other two muscles. When the gastrocnemius from an unoperated animal rather than a CCON muscle was used as a benchmark, slight increases were found for total nonpolar, polar, and plasmalogen fractions following denervation. The changes for individual lipid fractions were less definable, except for the significant increase for the unknown polar compound near the origin. This spot was noted in extracts from CCON and DEN muscles but not in untouched control muscle. The CCON gastrocnemius muscle is therefore a poor control for determining effects of denervation on lipid levels and perhaps other biochemical parameters as well.     

Ultrastructural changes in the connective tissue of skeletal muscles following denervation]

The ultrastructural changes found in the endomysium of rats after denervation of the diaphragm and m. plantaris were studied. Within the first week after crossing the peripheral nerve in the nedomysium there appeared an increased amount of neutrophils and monocytes as well as phagocytic material in the cytoplasm of histocytes. Activization of the cytoplasm of fibroblasts which manifested itself in the appearance of numerous vesicles and multiple free and bound ribosomes was detected by the end of the second and the beginning of the third weeks after denervation. At the same period eosinophils invaded the endomysium and became closely surrounded by numerous collagenic fibres. After reparation of neuromuscular synapses these changes disappeared. On the basis of these results and others founded in previous studies of denervated and reinnervated skeletal muscles the authors consider these changes in the endomysium appearing under the above experimental conditions to be manifestations of metabolic interrelations between the endomysium connective tissue and muscle fibres.     

Effect of temporary denervation on the development

Summary The influence of the motoneurone on the morphogenesis of the postsynaptic membrane of the myoneural junction was studied by denervation and subsequent re-innervation of the rat tibialis anterior muscles. This was effected by compressing the sciatic nerve at different stages of myoneural morphogenesis during the first month after birth. Changes in the postsynaptic structure were followed by histochemical demonstration of acetylcholinesterase (E.C. 3.1.1.7.) axtivity.Compression of the nerve brought development of the postsynaptic membrane to a standstill for about two to three weeks, the delay being greater in older rats. Subsequent structural development after re-innervation, although delayed for about two to three weeks, continued in the same way as in the controls.These observations indicate that the motoneurone exerts a long-lasting trophic stimulus on the development of the postsynaptic membrane of the muscle fibre and that this morphogenetic action continues throughout the structural maturation of the myoneural junction in the rat.     

Effect of denervation on pigeon slow skeletal muscle

Summary The slow anterior latissimus dorsi muscle (ALD) of the pigeon was denervated surgically and examined after varying post-operative intervals. Muscles were studied with respect to changes in weight, histological and ultrastructural alterations, and changes in size and number of fibers. The weights of the denervated muscles increased over the contralateral control, reaching a maximum hypertrophy in the first 18 days, but the hypertrophy persisted for several months. The fibers of the denervated muscle did not hypertrophy. They showed a gradation in size from the posterior to the anterior border, with the fibers in the anterior third of the muscle being the smallest. After measuring cross-sectional sizes from the anterior, middle, and posterior thirds of the muscle, the overall fiber change was one of atrophy.Morphologically, the fibers showed various signs of pathological changes, including nuclear proliferation, swelling and migration away from the sarcolemmal position, vacuolation, myofibril degeneration, connective-tissue infiltration and replacement of the fibers, and regenerative activities in the form of budding and myoblast formation. A condition termed a peripheral rim of degeneration is described. Although many abnormal conditions were found in these denervated muscles, much of the muscle appeared normal; the neurotrophic relationship of slow muscle is discussed.This investigation was supported in part by a Public Health Service Fellowship, 2 F 2 NB 35, 582, from the National Institute of Neurological Diseases and Stroke, and by an Ohio University Research Grant to R. Hikida; and a grant 5 RO 1 AN 10856 from the National Institute of Arthritis and Metabolic Diseases to W. Bock.The authors wish to acknowledge gratefully the skillful technical assistance of Mr. Lawrence Mezza and Miss Sally Mitchell.     

Myosin isoforms of skeletal muscles in development

The latest data are reviewed concerning identification of myosin from the skeletal muscle during embryonic and postnatal development in vertebrates. The data are given on the composition of light subunits and specificity of heavy chains of the early isoforms obtained by electrophoresis, peptide mapping, DNA-RNA hybridization, as well as immunological methods with poly-and monoclonals. The substitution of embryonic heavy chains by neonatal and definitive ones is discussed. The following items are also considered: early isoforms of the fast and slow myosin types and, in particular, endogenous program directing the muscle development and protein synthesis towards the "fast phenotype", which is modulated by neurostimulation and other physiological factors inducing slow myosin type. The enzymatic activity of the early isoforms and its physiological importance in embryogenesis are discussed.     

Effect of denervation on loss of ions in chick skeletal muscle

Leaching behaviour of chick gastrocnemius muscle has been studied with respect to the loss of Na+, K+ and Ca2+ ions in a donor-solvent (muscle-water) system under normal as well as denervated conditions. An attempt has been made to explain the alterations in the rate of electrolytic loss in terms of membrane dysfunctions induced as a result of loss of neural control.     

Ribosome biogenesis in skeletal development and the pathogenesis of skeletal disorders

The skeleton affords a framework and structural support for vertebrates, while also facilitating movement, protecting vital organs, and providing a reservoir of minerals and cells for immune system and vascular homeostasis. The mechanical and biological functions of the skeleton are inextricably linked to the size and shape of individual bones, the diversity of which is dependent in part upon differential growth and proliferation. Perturbation of bone development, growth and proliferation, can result in congenital skeletal anomalies, which affect approximately 1 in 3000 live births [1]. Ribosome biogenesis is integral to all cell growth and proliferation through its roles in translating mRNAs and building proteins. Disruption of any steps in the process of ribosome biogenesis can lead to congenital disorders termed ribosomopathies. In this review, we discuss the role of ribosome biogenesis in skeletal development and in the pathogenesis of congenital skeletal anomalies. This article is part of a Special Issue entitled: Role of the Nucleolus in Human Disease.