Acetylcholine is released at the neuromuscular junction and binds to a nicotinic receptor, causing an action potential to fire down the T tubules. The voltage change from this is sensed by the Sarcoplasmic Reticulum which then releases Ca2+ ions into the cytosol. The Ca2+ ions bind to troponin which moves tropomyosin from the active sites of the actin filament. Once the active sites are revealed, myosin quickly forms a cross bridge and begins contraction.
ACh (acetylcholine) binds to receptors at the NMJ (neuromuscular junction) to induce contraction of muscle.
A signal is generated in the motor cortex of the brain, and travels down the spinal cord to the affected motor neurons. As the action potential travels down the axon of the final motor neuron, it causes calcium influx and exocytosis of acetylcholine-containing vesicles, releasing acetylcholine into the neuromuscular junction. From there, acetylcholine binds with receptors on the muscle fiber end plates, where it depolarizes the muscle fiber, causing contraction of the muscle.
The acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the motor end plate of the muscle cell. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out.
Alpha-Motor neurons release the neurotransmitter acetylcholine at a synapse called the neuromuscular junction. When the acetylcholine binds to acetylcholine receptors on the muscle fiber, an action potential is propagated along the muscle fiber in both directions.
Acetylcholine release is necessary for skeletal muscle contraction, because it serves as the first step in the process, enabling the subsequent cross-bridge formation. A muscle's ability to contract depends on the formation of cross-bridges between myosin & actin filaments. A drug that blocks acetylcholine release would interfere with this cross-bridge formation and prevent muscle contraction
Alpha-Motor neurons release the neurotransmitter acetylcholine at a synapse called the neuromuscular junction. When the acetylcholine binds to acetylcholine receptors on the muscle fiber, an action potential is propagated along the muscle fiber in both directions.
triggers neurotransmitter secretion, removes contraction inhibitor, and binds with troponin.
Triggering of the muscle action potential occurs after acetylcholine binds to chemically-gated channels in the end plate membrane.
Actin Changes ShapeApexMyosin binds to ActinAPEX
Actin Changes ShapeApexMyosin binds to ActinAPEX
Actin changes shape.
Acetylcholine (ah-Seh-til-KO-leen) is the organic molecule that triggers muscle contractions in humans. Acetylcholine acts on both the central nervous system (CNS) and on the peripheral nervous system (PNS). It is also the principal neurotransmitter in autonomic ganglia.