what affect does acetylcholine have on the sarcolemma
Neuromuscular junction Muscles require innervation to functionâ€”and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Sarcoplasmic reticulum SERCA consists of 13 subunits (labelled M1-M10, N, P and A). Calcium ions bind to the M1-M10 subunits (which are located within the membrane), whereas ATP binds to the N,P and A subunits (which are located outside the SR). When 2 calcium ions, along with a molecule of ATP, bind to the cytosolic side of the pump (i.e the region of the pump outside the SR), the pump opens. This occurs because ATP (which contains three phosphate groups) releases a single phosphate group (becoming adenosine diphosphate). The released phosphate group then binds to the pump, causing the pump to change shape. This shape change causes the cytosolic side of the pump to open, allowing the two Ca2+ to enter. The cytosolic side of the pump then closes and the sarcoplasmic reticulum side opens, releasing the Ca2+ into the SR.[6]