Sarcolemma
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The sarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli.
Alterations in the sarcolemmal membrane stability and repair system can lead to muscular dystrophy. The mechanism of muscular dystrophy is lack of functional dystrophin. This means that the sarcolemma is not attached to the cytoskeleton. Therefore during muscle contraction, the sarcolemma is not synchronized with the interior of the cell. The looseness of the sarcolemma permits membrane calcium channels to open. The rise in internal calcium ions causes activation of the proteolytic enzyme calpain, which digests proteins including contractile proteins, rendering the muscle much weaker.
The sarcolemma invaginates into the cytoplasm of the muscle cell, forming membranous tubules called transverse tubules (t-tubules). Sarcoplasmic reticulum is the enlargement of smooth endoplasmic reticulum found in muscle cells on either side of the transverse tubules. The triad of transverse tubules surrounded by two smooth ER cisternae transmit altered membrane permeability down the tubules. The nuclei lie just adjacent to the sarcolemma, at the periphery of the fiber.
This membrane is extensible and encloses the contractile substance of a muscle fiber.
See also
it:Sarcolemmavi:Màng sợi cơ
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

