Degenerative changes at the neuromuscular junctions of red, white and intermediate muscle fibers

1979 ◽  
Vol 43 (2) ◽  
pp. 205-222 ◽  
Author(s):  
Dallas L. Pulliam ◽  
Ernest W. April
1975 ◽  
Vol 38 (6) ◽  
pp. 1390-1394 ◽  
Author(s):  
F. Emonet-Denand ◽  
Y. Laporte

Of 32 cat peroneus brevis spindles, 23 (72%) were found to be supplied by a least 1 skeletofusimotor or beta-axon. A motor axon was identified as skeletofusimotor when repetitive stimulation of it elicited both the contraction of extrafusal muscle fibers and as acceleration of the discharge of primary ending, which persisted after selective block of the neuromuscular junctions of extrafusal muscle fibers. The block was obtained by stimulating single axons at 400-500/s for a few seconds. Of 135 axons supplying extrafusal muscle fibers, 24 (18%) were shown to be beta-axons; 22 beta-axons had conduction velocities ranging from 45 to 75 m/s. All but three beta-axons increased the dynamic sensitivity of primary endings. Beta-innervated spindles may also be supplied by dynamic gamma-axons.


Author(s):  
Б. В. Борисевич ◽  
В. В. Лісова ◽  
М. С. Криштоп

Представлено результати гістологічних дослі-джень нирок і міокарду курей, які загинули від інфек-ційного ларинготрахеїту. Встановлено, що в нирках реєструються розлади кровообігу в вигляді розши-рення та переповнення кров’ю кровоносних судин строми органа, екстракапілярний серозний гломеру-лонефрит і дистрофічні зміни та руйнування епіте-лію канальців. У міокарді провідною патологією була зерниста дистрофія м’язових клітин. Окрім того реєструвалися фрагментація та дезорієнтація м’язових волокон. У епікарді та ендокарді мікроско-пічних змін не було. The results of histological studies of kidneys and myocardium of chickens that died of infectious laryngotracheitis have been shown. It was found that circulatory disorders in the form of expansion and overflow of blood with blood vessels of body stroma, extra serosal capillary glomerulonephritis and degenerative changes and destruction of epithelial tubules are registered in the kidneys. In the myocardium the leading pathology was granular dystrophy of muscle cells. In addition, fragmentation and disorientation of muscle fibers was registered. In the epicardium and endocardium there were no microscopic changes.


1977 ◽  
Vol 40 (4) ◽  
pp. 836-843 ◽  
Author(s):  
S. Carbonetto

1. Neuromuscular transmission was studied in the extensor digitorum-longus muscle of dystrophic mice (strain 129/ReJ) by means of intracellular recording techniques. 2. In a large population of normal and dystrophic muscle fibers tested, the incidence of transmission failure was about 2% and showed no significant difference between the two groups. 3. Quantal size and quantum content of dystrophic junctions were found to be normal. This was true even of nerve terminal on apparently atrophied muscle fibers. 4. The facilitation ratio at dystrophic junctions was not significantly different from normal. 5. Dystrophic neuromuscular junctions exhibited an abnormality high frequency of giant spontaneous potentials. Application of tetrodotoxin (10(-6) M) and curare (10(-6) M) indicated that these potentials were caused by impulse-independent release of acetylcholine. 6. Neuromuscular transmission in dystrophic mice was found functionally normal and unrelated to the degenerative state of the muscle.


Author(s):  
Teet Seene ◽  
Maria Umnova ◽  
Priit Kaasik

The aim of our research was to examine whether there are differences in the morphology of neuromuscular junctions of different types of muscle fibers in rodents, and after their adaptation to six weeks endurance exercise training. After 5-day acclimation, Wistar rats were subjected to run with the speed 35 m/min during 6 week, 5 days per week and the training volume reached 60 min per day. Muscle samples for ultrastructural studies were fixed, dehydrated and embedded in Epon-812. Ultra-thin sections were cut from longitudinally and transversely oriented blocs, using 4 blocks from each animal. The area of axon terminals on fast- twitch fibers is 1.5 time large (p<0.001) and the perimeter of terminals is 1.7 time large in comparison with slow- twitch oxidative fibers (p<0.001) in control group. There are correlation between cross-sectional area of different muscle fibers and length of axon terminals (r=0.72), between cross-sectional area and with of axon terminal (r=-0.62), and between turnover rate of contractile proteins and length of axon terminal (r=0.75). Fast remodeling of synapse on oxidative and oxidative-glycolytic muscle fibers during endurance training seems to guarantees the intensive renewal of the structures of muscle fibers with higher oxidative capacity.


Micron ◽  
2015 ◽  
Vol 71 ◽  
pp. 7-13 ◽  
Author(s):  
Heloisa Deola Confortim ◽  
Leslie Cazetta Jerônimo ◽  
Lígia Aline Centenaro ◽  
Patrícia Fernanda Felipe Pinheiro ◽  
Rose Meire Costa Brancalhão ◽  
...  

1985 ◽  
Vol 101 (3) ◽  
pp. 735-743 ◽  
Author(s):  
L Anglister ◽  
U J McMahan

In skeletal muscles that have been damaged in ways which spare the basal lamina sheaths of the muscle fibers, new myofibers develop within the sheaths and neuromuscular junctions form at the original synaptic sites on them. At the regenerated neuromuscular junctions, as at the original ones, the muscle fibers are characterized by junctional folds and accumulations of acetylcholine receptors and acetylcholinesterase (AChE). The formation of junctional folds and the accumulation of acetylcholine receptors is known to be directed by components of the synaptic portion of the myofiber basal lamina. The aim of this study was to determine whether or not the synaptic basal lamina contains molecules that direct the accumulation of AChE. We crushed frog muscles in a way that caused disintegration and phagocytosis of all cells at the neuromuscular junction, and at the same time, we irreversibly blocked AChE activity. New muscle fibers were allowed to regenerate within the basal lamina sheaths of the original muscle fibers but reinnervation of the muscles was deliberately prevented. We then stained for AChE activity and searched the surface of the new muscle fibers for deposits of enzyme they had produced. Despite the absence of innervation, AChE preferentially accumulated at points where the plasma membrane of the new muscle fibers was apposed to the regions of the basal lamina that had occupied the synaptic cleft at the neuromuscular junctions. We therefore conclude that molecules stably attached to the synaptic portion of myofiber basal lamina direct the accumulation of AChE at the original synaptic sites in regenerating muscle. Additional studies revealed that the AChE was solubilized by collagenase and that it remained adherent to basal lamina sheaths after degeneration of the new myofibers, indicating that it had become incorporated into the basal lamina, as at normal neuromuscular junctions.


1976 ◽  
Vol 54 (8) ◽  
pp. 1314-1325 ◽  
Author(s):  
Kristine H. Atkinson ◽  
Burr G. Atkinson ◽  
Peter A. Merrifield

The appearance of differentiated tissue types after amputation of Rana catesbeiana tadpole tail follows a precise chronological order. Migrating epithelial cells invest the wound within 3 days. Blastemal cells accumulate under the distal epithelium in the early stages when tissue debris is cleared away, then by day 11 notochordal outgrowth and nerve axon replacement predominate in the highly vascularized blastema.Fusion of the myoblasts to form the first detectable myotubes occurs in the proximal region of the regenerate by day 14. Myogenesis proceeds distally with myotubes present under the epithelium of the distal tip of the regenerate at day 19. After day 22 further increase in tail musculature is probably due to the growth of fibers already formed. At day 22 the new muscle fibers begin to anastomose with the healed ends of the old fibers. From 35 to 48 days the major remaining difference from control tissues is the size and extent of the regenerated muscle fibers; capillaries, axons, epidermis and dermis, and neuromuscular junctions are morphologically indistinguishable from unregenerated tissues.


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