What Stimulates a Muscle to Contract

Muscle contraction is controlled by the axons of motor neurons, which form synapses with myofibres called neuromuscular connection. The action potentials on axons trigger the fusion of acetylcholine-containing synaptic vesicles with the plasma membrane, which leads to the release of acetylcholine into the space between axon and myofiber. Acetylcholine binds to acetylcholine receptors, the cationic channels, which leads to the opening of these channels and the generation of a new action potential in the myofiber plasma membrane (the sarcolemma). Throughout smooth muscle, calcium-bound CaM then binds to MLCK and stimulates MLC phosphorylation, resulting in muscle contraction. The need for MLCK has been demonstrated in MLCK knockout mice where smooth muscle MLC cannot be phosphorylated by other kinases (He et al. 2008; Zhang et al., 2010). Dephosphorylation of MLC is catalyzed by mlCP and a myosin complex targeting the MYPT1 protein and PP1 phosphatase and leads to relaxation. In the stomach muscle, rhythmic contractions are due to the activity of pacemaker cells, but activation of tension-controlled calcium channels can trigger the entry and contraction of calcium. Sympathetic nerves run along smooth vascular muscles and can release stimuli such as acetylcholine, norepinephrine, angiotensin, and endothelin. In addition, circulating blood factors such as cytokines and diffusible factors such as nitric oxide can also act on plasma membrane receptors or cross the plasma membrane to regulate pathways that control intracellular calcium levels.

Activation of receptor-fed channels (ROC) also causes an influx of calcium, allowing for additional release of calcium from intracellular reserves. GPCRs allow PLCĪ² to generate IP3s, which release calcium via IP3Rs. In smooth vascular muscles and circular smooth muscles of the intestine, the main isoform is IP3R1. Note, however, that there is some heterogeneity. In the smooth longitudinal muscles of the intestine, RyRs are expressed instead of IP3Rs. Agonists such as cholecystokinin bind to the GPCR CHOLECYSTOKININ A receptor (CCK-AR), which activates phospholipase A2, which in turn produces arachidonic acid. Arachidonic acid (AA) can also be produced by dividing DAG. AA activates chloride channels that depolarize the cell membrane and allow the opening of voltage-dependent calcium channels and an initial influx of calcium. This calcium can either act directly on the RyR that causes the ICRC, or allow the release of cyclic ADP ribose that interacts with the RyRs to improve the ICRC.

The release of Ca2+ from the sarcoplasmic reticulum and the interaction of actin and myosin lead to muscle contraction. Figure 3.2. (A) A motor neuron is a neuronal cell that innervates a series of muscle fibers. It consists of a body, a tree of relatively short dendrites and a long axon with terminal branches at its end. Each branch forms a synapse with a target muscle fiber. (B) The neuromuscular synapse is a complex anatomical structure composed of a presynaptic neuronal fiber, synaptic cleft and postsynaptic muscle fiber. An action potential entering along the nerve fiber always creates an action potential on the muscle fiber: this action is said to be mandatory. The action potential of the muscle fiber spreads at a rate of 3 to 5 m / s along the muscle membrane (the sarcolemma) and in the tubules T (at the intersection of ligaments A and I) (Figure 8).

The latter, flanked by the sarcoplasmic reticulum and forming a complex of triads, transmits the action potential within the muscle fiber; This action potential causes the signal to be transduction by ryanodine receptors that release calcium ions. The calcium ions then bind to the troponin subunits, resulting in a conformational change in the tropomyosin and actin-helix configurations. In another calcium-dependent process that requires ATP, transverse bridges form between thick, thin filaments. Sliding thin filaments of actin over thick filaments of myosin creates muscle contraction. The shortening of the sarcomeres and band I during contraction is not due to a change in the absolute length of the filaments, but to the slippage of the filaments. The contraction stops when calcium is removed from the sarcoplasmic reticulum by active transport. .