The labelling of motor end-plates in skeletal muscle of mice with 125I tetanus toxin

1977 ◽  
Vol 298 (1) ◽  
pp. 37-42 ◽  
Author(s):  
A. Wernig ◽  
H. St�ver ◽  
D. Tonge
Keyword(s):  
Skeletal Muscle ◽  
Tetanus Toxin ◽  
Motor End Plates

Rapid dilation of arterioles with single contraction of hamster skeletal muscle

2006 ◽  
Vol 290 (1) ◽  
pp. H119-H127 ◽  
Author(s):  
Jurgen W. G. E. VanTeeffelen ◽  
Steven S. Segal
Keyword(s):  
Skeletal Muscle ◽  
Muscarinic Receptor ◽  
Muscle Blood Flow ◽  
Rapid Onset ◽  
Receptor Activation ◽  
Retractor Muscle ◽  
Time Integral ◽  
Exercise Onset ◽  
Tension Time ◽  
Motor End Plates

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.

scholarly journals CHOLINESTERASES AND MOTOR END-PLATES IN DEVELOPING DUCK SKELETAL MUSCLE

1965 ◽  
Vol 13 (7) ◽  
pp. 559-565 ◽  
Author(s):  
K. S. KHERA ◽  
Q. N. LAHAM
Keyword(s):  
Skeletal Muscle ◽  
Nerve Fibers ◽  
Diisopropyl Fluorophosphate ◽  
Thigh Muscles ◽  
Motor End Plates ◽  
Subneural Apparatus

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.

Disorders Caused by Botulinum Toxin and Tetanus Toxin

2017 ◽  
Author(s):  
Carl E. Stafstrom
Keyword(s):  
Skeletal Muscle ◽  
Botulinum Toxin ◽  
Motor Neurons ◽  
Tetanus Toxin ◽  
Botulinum Neurotoxin ◽  
Acetylcholine Release ◽  
Neuromuscular Junctions ◽  
Muscle Rigidity ◽  
Inhibitory Neurotransmitters ◽  
Central Synapses

Anaerobic organisms of the genus Clostridia (C) can cause significant human disease. Exotoxins secreted by C botulinum and C tetani cause botulism and tetanus, respectively (summarized in Table 156.1). Botulinum neurotoxin causes neuromuscular blockade by interfering with vesicular acetylcholine release, leading to cholinergic blockade at the neuromuscular junctions of skeletal muscle, and consequently, symmetric flaccid paralysis. Tetanus toxin prevents release of inhibitory neurotransmitters at central synapses, leading to overactivity of motor neurons and muscle rigidity and spasms. This chapter reviews clinical features of botulism and tetanus and discusses their pathophysiological basis.

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