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∙ 9y agoChemically gated Na+ ions.
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∙ 9y agoAcetylcholine binding causes nicotinic acetylcholine receptors on the folded sarcolemma to open, allowing the influx of sodium ions into the muscle cell. This initiates an action potential that propagates along the sarcolemma and into the T-tubules, triggering muscle contraction.
Acetylcholine binds to receptors on the postsynaptic membrane, leading to a change in ion permeability and generation of a signal. Acetylcholine that is not bound is rapidly broken down by the enzyme acetylcholinesterase. The resulting breakdown products are recycled for later use in the presynaptic neuron.
The signal to excite a muscle cell involves the release of acetylcholine from the motor neuron into the synaptic cleft at the neuromuscular junction. Acetylcholine diffuses across the synaptic cleft and binds to receptors on the muscle cell membrane, leading to depolarization and muscle contraction. This process is crucial for transmitting signals from the nervous system to the muscle for movement.
Exocytosis. As a result of the influx of Calcium ions, the synaptic vesicles transport the neurotransmitter Ach (Acetylcholine) to the presynaptic membrane, the vesicles fuse to the membrane, and the neurotransmiffer, Ach, diffuses. Once the neurotransmitters cross the synaptic cleft, they bind to the receptors on the post synaptic membrane. Hope it helps a bit.
Calcium enters through the voltage-gate and triggers the release of transmitter. " the entry of calcium through voltage-gated calcium channels causes synaptic vesicles to fuse with the presynaptic plasma membrane and release the neurotransmitter acetylcholine into the synaptic cleft. Acetylcholine diffuses across the cleft and binds to muscle acetylcholine receptors, causing depolarization and an action potential that travels throughout the length of the muscle cell triggering muscle contraction. "
When an action potential reaches the end of an axon, it triggers the release of neurotransmitters from synaptic vesicles into the synaptic cleft. These neurotransmitters then bind to receptors on the adjacent neuron, stimulating a new action potential to propagate the signal to the next neuron.
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.
Acetylcholine binds to receptors on the postsynaptic membrane, leading to a change in ion permeability and generation of a signal. Acetylcholine that is not bound is rapidly broken down by the enzyme acetylcholinesterase. The resulting breakdown products are recycled for later use in the presynaptic neuron.
The contraction mechanism in a skeletal muscle cell is initiated by an action potential traveling down the motor neuron and releasing acetylcholine at the neuromuscular junction. Acetylcholine binds to receptors on the muscle cell membrane, causing depolarization and the propagation of an action potential along the sarcolemma. This triggers the release of calcium ions from the sarcoplasmic reticulum, leading to the sliding of actin and myosin filaments and muscle contraction.
Neuromuscular
The signal to excite a muscle cell involves the release of acetylcholine from the motor neuron into the synaptic cleft at the neuromuscular junction. Acetylcholine diffuses across the synaptic cleft and binds to receptors on the muscle cell membrane, leading to depolarization and muscle contraction. This process is crucial for transmitting signals from the nervous system to the muscle for movement.
1. Nerve impulse reaches synaptic terminal. 2. Synaptic vesicles move to and merge with the presynaptic cell membrane of the motor neuron. 3. Acetylcholine is released into and diffuses across the synaptic cleft. 4. Acetylcholine binds to receptors on the postsynaptic cell membrane of the muscle fiber.
nerve impulse
Exocytosis. As a result of the influx of Calcium ions, the synaptic vesicles transport the neurotransmitter Ach (Acetylcholine) to the presynaptic membrane, the vesicles fuse to the membrane, and the neurotransmiffer, Ach, diffuses. Once the neurotransmitters cross the synaptic cleft, they bind to the receptors on the post synaptic membrane. Hope it helps a bit.
During Parasympathetic action when acetlcholine is released in the sphincter muscles then the M3 muscarinic receptors stimulate Gq protein and this in turn activate Phospholipase C (PLC). PLC then cleaves the phospholipid. In the process, phosphatidylinositol 4,5-bisphosphate (PIP2) is cleaved into diacyl glycerol (DAG) and inositol 1,4,5-triphosphate (IP3). DAG remains bound to the membrane and IP3 is released as a soluble structure in the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly the calcium channels in the endoplasmic reticulum (ER). These channels are specific to calcium and allow only the passage of calcium to move through. This causes the cytosolic concentration of calcium to increase and cause the cascade of contractile machinery and the spinchter will contract and tighten up.
Calcium enters through the voltage-gate and triggers the release of transmitter. " the entry of calcium through voltage-gated calcium channels causes synaptic vesicles to fuse with the presynaptic plasma membrane and release the neurotransmitter acetylcholine into the synaptic cleft. Acetylcholine diffuses across the cleft and binds to muscle acetylcholine receptors, causing depolarization and an action potential that travels throughout the length of the muscle cell triggering muscle contraction. "
It varies: In the somatic system (skeletal muscle) and parasympathetic branch of the autonomous nervous system (smooth & cardiac muscle) it is usually acetylcholine. In the sympathetic branch of the autonomous nervous system (smooth & cardiac muscle) it is usually norepinephrine (also called noradrenaline). There are exceptions, but this is the general rule.
When an action potential reaches the end of an axon, it triggers the release of neurotransmitters from synaptic vesicles into the synaptic cleft. These neurotransmitters then bind to receptors on the adjacent neuron, stimulating a new action potential to propagate the signal to the next neuron.