Ultrastructure of motor end-plates during pharmacologically-induced degeneration and subsequent regeneration of skeletal muscle

1975 ◽  
Vol 4 (2) ◽  
pp. 141-155 ◽  
Author(s):  
Isa Jirmanov�
2006 ◽  
Vol 290 (1) ◽  
pp. H119-H127 ◽  
Author(s):  
Jurgen W. G. E. VanTeeffelen ◽  
Steven S. Segal

Skeletal muscle blood flow increases rapidly with exercise onset, but little is known of where or how the rapid onset of vasodilation (ROV) is governed within the microcirculation. In the retractor muscle of anesthetized hamsters ( n = 26), we tested the following: 1) where in the resistance network ROV occurred, 2) how microvascular responses were affected by the duration of contraction, and 3) whether ROV involved muscarinic receptor activation. Single tetanic contractions were evoked using supramaximal field stimulation (100 Hz) to depolarize motor end plates. In response to a 200-ms contraction, red blood cell (rbc) velocity ( Vrbc) in feed arteries (FA; rest: 17.8 ± 2 mm/s) increased within 1 s; a transient first peak (P1; 50 ± 7% increase) occurred at ∼5 s; and a second peak (P2; 50 ± 15% increase) occurred at ∼15–20 s. For vasodilation, P1 increased in frequency from proximal FA (2/7) and 1A arterioles (2/7) to distal 2A (4/7) and 3A (7/8) arterioles ( P < 0.05). Relative to resting (and maximal, 10 μM sodium nitroprusside) diameters, P1 increased from proximal (FA, 3 ± 2% from 57 ± 5 μm) to distal (3A, 27 ± 6% from 14 ± 1 μm) vessel branches ( P < 0.05). P2 was manifest in all vessels and increased relative to resting diameters from FA (11 ± 3%) to 3A (36 ± 6%) branches ( P < 0.01). Extending a contraction from 200 to 1,000 ms (tension × time integral from 17 ± 2 to 73 ± 4 mN/mm2 × s) increased P1 and P2 for Vrbc and for diameter ( P < 0.05) while reducing the time of onset for P2 ( P < 0.05). Superfusion with atropine (10 μM) attenuated P1 of vasodilation (200 ms contraction) from 26 ± 8% to 6 ± 2% ( n = 7 across branches; P < 0.05) and reduced the diameter × time integral by 46 ± 13% ( P < 0.05) without changing P2. We conclude that ROV in the hamster retractor muscle is initiated in distal arterioles, increases with the duration of muscle contraction, and involves muscarinic receptor activation.


1965 ◽  
Vol 13 (7) ◽  
pp. 559-565 ◽  
Author(s):  
K. S. KHERA ◽  
Q. N. LAHAM

End-plates in the thigh muscles of duck embryos were first recognized with myristoylcholine as substrate at the 19th day of incubation. Each appeared as a cholinesterase-positive dot surrounded by a small halo which rapidly increased in size during the 20th and 21st days. The endplates were usually oval in shape, averaging 33 µ x 25 µ with a subneural apparatus 5-12µ wide. The latter contained refringent lamellas arranged transversely in a palisade fashion. From the 21st day to the day of hatching (27-29 days) the number of end-plates progressively increased. After hatching, the myristoylcholine-reacting end-plates were difficult to locate. With acetylthiocholine as substrate, the embryonal end-plates were not demonstrable; however, the posthatched tissues showed numerous end-plates. The nerve trunks and nerve fibers gave a faintly positive myristoylcholine reactions in all stages after the 19th day of incubation. On the basis of the effects of eserine and diisopropyl fluorophosphate, the structures reacting with myristoylcholine and acetylthiocholine contained specific chohinesterase. The end-plates containing nonspecific cholinesterase also appeared on the 19th day of incubation and appeared to increase gradually in number until the 15th postembryonic day; thereafter they seemed to decrease.


Development ◽  
1986 ◽  
Vol 92 (1) ◽  
pp. 1-10
Author(s):  
Adarshk Gulati

Autotransplantation of rat extensor digitorum longus muscle results in initial myofibre degeneration and subsequent regeneration from precursor myosatellite cells. To determine what effect a reinjury would have on the regenerative response, in the present,study, once transplanted and regenerated muscles were reinjured by reautotransplantion. In rats, four weeks after initial transplantation, when the regeneration was complete, the extensor digitorum longus muscle was transplanted again and the pattern of regeneration in reautotransplanted and once auto transplanted muscles was compared. Muscles were analysed 2, 4, 7, 14 and 30 days after autotransplantation and reautotransplantation. Both autotransplanted and reautotransplanted muscles underwent degeneration and regeneration; however, the pattern of regeneration in these two transplants was quite different. In autotransplants, a thin myogenic zone, marked by activated myoblasts, was first seen at 4 days. By 7 days the width of myogenic zone increased but still many degenerating myofibres were present in the central region of the muscle. By 14 days the muscle was filled with regenerated myotubes and myofibres. The reautotransplanted muscles underwent similar regenerative events; however, the rate of regeneration was considerably faster. The myogenic zone was apparent as early as 2 days and was much larger at 4 days, and by 7 days the entire muscle was filled with regenerated myotubes and myofibres which matured at later time intervals. Furthermore, the decrease in muscle weight in reautotransplanted muscles was not as much as that seen after autotransplantation. These findings reveal that not only is skeletal muscle capable of regeneration after a second injury, but the rate of this regeneration is much faster. This increased rate and recovery may be due to a conditioning effect of the first injury.


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