transverse tubules allows the nerve impulses that initiate muscle contraction to travel along the sarcolemma.
transverse tubules allows the nerve impulses that initiate muscle contraction to travel along the sarcolemma.
what allows the nerve impulses that initiate muscle contraction to travel along the sarcolemma?
transverse tubules
excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract. in skeletal muscle, excitation–contraction coupling relies on a direct coupling between key proteins, the sarcoplasmic reticulum (sr) calcium release channel (identified as the ryanodine receptor, ryr) and voltage-gated l-type calcium channels (identified as dihydropyridine receptors, dhprs). dhprs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the ryrs reside across the sr membrane. the close apposition of a transverse tubule and two sr regions containing ryrs is described as a triad and is predominantly where excitation–contraction coupling takes place. excitation–contraction coupling occurs when depolarization of skeletal muscle cell results in a muscle action potential, which spreads across the cell surface and into the muscle fiber's network of t-tubules, thereby depolarizing the inner portion of the muscle fiber. depolarization of the inner portions activates dihydropyridine receptors in the terminal cisternae, which are in close proximity to ryanodine receptors in the adjacent sarcoplasmic reticulum. the activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (involving conformational changes that allosterically activates the ryanodine receptors). as the ryanodine receptors open, is released from the sarcoplasmic reticulum into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium spark. note that the sarcoplasmic reticulum has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin. the near synchronous activation of thousands of calcium sparks by the action potential causes a cell-wide increase in calcium giving rise to the upstroke of the calcium transient. the released into the cytosol binds to troponin c by the actin filaments, to allow crossbridge cycling, producing force and, in some situations, motion. the sarco/endoplasmic reticulum calcium-atpase (serca) actively pumps back into the sarcoplasmic reticulum. as declines back to resting levels, the force declines and relaxation occurs.
muscle contraction
a neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber. it is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. the sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction. once it reaches the terminal bouton, the action potential causes a ion influx into the terminal by way of the voltage-gated calcium channels. the influx causes synaptic vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. as a result, the sarcolemma reverses polarity and its voltage quickly jumps from the resting membrane potential of -90mv to as high as +75mv as sodium enters. the membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. this rapid fluctuation is called the end-plate potential the voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. these voltage-gated channels are sodium and potassium specific and only allow one through. this wave of ion movements creates the action potential that spreads from the motor end plate in all directions. if action potentials stop arriving, then acetylcholine ceases to be released from the terminal bouton. the remaining acetylcholine in the synaptic cleft is either degraded by active acetylcholine esterase or reabsorbed by the synaptic knob and none is left to replace the degraded acetylcholine.
muscle contraction