Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation

• Published in: Journal of applied physiology (1985) 2003-06, Vol.94 (6), p.2494-2501
• Main Authors: Mense, S, Simons, D. G, Hoheisel, U, Quenzer, B
• Format: Article
• Language: English
• Subjects: Acetylcholine - metabolism; Animals; Biological and medical sciences; Cholinesterase Inhibitors - administration & dosage; Electric Stimulation; Enzymes; Fundamental and applied biological sciences. Psychology; Hypotheses; Injections, Intramuscular; Isoflurophate - administration & dosage; Male; Motor Endplate - metabolism; Muscle Contraction; Muscle Fibers, Skeletal - pathology; Muscle, Skeletal - innervation; Muscular system; Myofascial Pain Syndromes - chemically induced; Myofascial Pain Syndromes - etiology; Myofascial Pain Syndromes - pathology; Myofascial Pain Syndromes - physiopathology; Neuromuscular Junction - physiology; Rats; Rats, Sprague-Dawley; Rodents; Striated muscle. Tendons; Vertebrates: osteoarticular system, musculoskeletal system
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00727.2002

1  Department of Anatomy and Cell Biology III, Heidelberg University, D-69 120 Heidelberg; 3  Department of Pharmacology and Toxicology, Kiel University, D-24 105 Kiel, Germany; and 2  Department of Rehabilitation Medicine, Emory University, Atlanta, Georgia 30322 In skeletal muscle, a local increase of acetylcholine (ACh) in a few end plates has been hypothesized to cause the formation of contraction knots that can be found in myofascial trigger points. To test this hypothesis in rats, small amounts of an acetylcholinesterase inhibitor [diisopropylfluorophosphate (DFP)] were injected into the proximal half of the gastrocnemius muscle, and the muscle nerve was electrically stimulated for 30-60 min for induction of muscle twitches. The distal half of the muscle, which performed the same contractions, served as a control to assess the effects of the twitches without DFP. Sections of the muscle were evaluated for morphological changes in relation to the location of blocked end plates. Compared with the distal half of the muscle, the DFP-injected proximal half exhibited significantly higher numbers of abnormally contracted fibers (local contractures), torn fibers, and longitudinal stripes. DFP-injected animals in which the muscle nerve was not stimulated and that were allowed to survive for 24 h exhibited the same lesions but in smaller numbers. The data indicate that an increased concentration of ACh in a few end plates causes damage to muscle fibers. The results support the assumption that a dysfunctional end plate exhibiting increased release of ACh may be the starting point for regional abnormal contractions, which are thought to be essential for the formation of myofascial trigger points. dysfunctional end plate; contracture; contraction knots; myofascial trigger points