Calcim
T tubules
sarcoplasmic reticulum
When Ach enters the synaptic cleft (gap) it open chemically gated sodium channels that starts an action potential spreading through the sarcolemma of the myofibril. This action potential spreads down the T-tubules and "shocks" the sarcoplasmic reticulum into releasing calcium ions.
The Golgi Apparatus is a highly-folded membrane structure on the terminal portion of the endoplasmic reticulum. The Golgi is the final packaging and distribution station prior to release into the cytoplasm or loading into vesicles for extracellular transport.
phospholipase C
T tubules
The enlarged portion of sarcoplasmic reticulum on either side of a transverse tubule is called a terminal cisterna. These terminal cisternae play a vital role in the excitation-contraction coupling of skeletal muscle cells. They store and release calcium ions, which are essential for muscle contraction.
Calcium release from the sarcoplasmic reticulum initiates the contraction.
Terminal cisterns of the sarcoplasmic reticulum through the Rhynodine receptors release calcium into the skeletal muscle cell when stimulated by an action potential.
sarcoplasmic reticulum
action potential propagating down the T tubule
The T tubules conduct electrical impulses that stimulate calcium release from the sarcoplasmic reticulum.
When Ach enters the synaptic cleft (gap) it open chemically gated sodium channels that starts an action potential spreading through the sarcolemma of the myofibril. This action potential spreads down the T-tubules and "shocks" the sarcoplasmic reticulum into releasing calcium ions.
Jiefei Tong has written: 'Defects in the Ca2+ release channel of skeletal muscle sarcoplasmic reticulum that are associated with malignant hyperthermia and central core disease'
After death, respiration in organisms ceases to occur, depleting the corpse of oxygen used in the making of Adenosine triphosphate (ATP). ATP is no longer provided to operate the SERCA pumps in the membrane of the sarcoplasmic reticulum, which pump calcium ions into the terminal cisternae. This causes calcium ions to diffuse from the area of higher concentration (in the terminal cisternae and extracellular fluid) to an area of lower concentration (in the sarcomere), binding with troponin and allowing for crossbridging to occur between myosin and actin proteins. Unlike in a normal muscle contraction, after death the body is unable to complete the cycle and release the coupling between the myosin and actin, creating a perpetual state of muscular contraction, until the breakdown of muscle tissue by digestive enzymes during decomposition. As part of the process of decomposition, the myosin heads are eaten off by bacteria, allowing the muscle contraction to release and the body to relax.
It is the release of calcium from the sarcoplasmic reticulum that then binds with actin-myosin ATPase to cause contractions. Low calcium would first affect the release of acetylcholine from the pre-synaptic terminus.
D- contraction phase