Chemically gated sodium channels open up when neurotransmitters bind to receptors in the motor end plate. This causes an action potential along a muscle membrane or nerve cell.
Acetylcholine receptors are located on the motor end plate of the muscle cell membrane. This specialized region is where the nerve cell communicates with the muscle cell, allowing for the initiation of muscle contraction in response to acetylcholine binding to its receptors.
ACH is released at the end-plate potential. ACH diffuses into the sarcolemma, attaches to the receptors in the motor end plate and causes a change in the ions permeability that creates graded depolarization of the end-plate potential. Basically, it attaches to the receptors in the motor-end plate and creates the beginning process of triggering muscle contractions.
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.
When a neurotransmitter binds to its receptor on the motor endplate, it triggers the opening of ion channels in the postsynaptic membrane. This allows for the influx of ions, typically leading to depolarization of the muscle cell membrane and initiation of a muscle action potential. Subsequently, this leads to contraction of the muscle fiber.
The action potential is conducted into a skeletal muscle fiber by the depolarization of the motor end plate, which triggers the opening of voltage-gated sodium channels. This causes an influx of sodium ions into the muscle fiber, leading to depolarization and the initiation of muscle contraction.
When acetylcholine binds to receptors at the motor plate, this binding opens ligand-gated ion channels on the motor end plate, ions diffuse through the open ligand gated ion channels, and the flow of ions causes the motor end plate to reach threshold and an action potential is generated at the motor end plate.
An incoming action potential to an alpha motor neuron causes acetylcholine (Ach)release at the end plate, Ach binds to Ach receptors on the sarcolemma causing a sodium influx which causes depolarization.
The stimulus that travels from the motor neuron to skeletal muscle is an electrical signal called an action potential. This action potential causes the release of neurotransmitters, specifically acetylcholine, which then stimulates 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.
An activated neuron will send an action potential from upper motor neurons to lower motor neurons to effector organs. It is able to propagate the action potential to the motor end plate by release of neurotransmitters, chiefly acetylcholine. On the terminal bouton the action potential opens voltage gated calcium channels. There is an influx of calcium in the pre-synaptic cell and it pushes the vesicles that contain acetylcholine. These vesicles will pass through the synaptic cleft and bind to cholinergic receptors on the post synaptic neuron. Each vesicle has a miniature end plate potential of 0.5mV. In a normal action potential, it will depolarize the post synaptic motor neuron from -85mV to approximately 0-15mV. So that's approximately 180 vesicles.* The influx of neurotransmitters (primarily acetylcholine) will depolarize the motor end plate and propagate the action potential. *Threshold of an action potential is approximately -55mV so technically the minimum required to continue an action potential is around 60 vesicles.
muscle twitch
The response of a motor unit to a single action potential of its motor neuron is called a muscle twitch. This involves the contraction of all the muscle fibers within the motor unit in response to the stimulation from the motor neuron.
Acetylcholine receptors are located on the motor end plate of the muscle cell membrane. This specialized region is where the nerve cell communicates with the muscle cell, allowing for the initiation of muscle contraction in response to acetylcholine binding to its receptors.
ACH is released at the end-plate potential. ACH diffuses into the sarcolemma, attaches to the receptors in the motor end plate and causes a change in the ions permeability that creates graded depolarization of the end-plate potential. Basically, it attaches to the receptors in the motor-end plate and creates the beginning process of triggering muscle contractions.
The neuromuscular junction consists of the motor neuron terminal, synaptic cleft, and motor end plate on the muscle fiber. When an action potential reaches the motor neuron terminal, it triggers the release of acetylcholine into the synaptic cleft. Acetylcholine then binds to receptors on the motor end plate, leading to muscle contraction.
Depolarization at the motor end plate upon arrival of action potentials triggers the release of neurotransmitter acetylcholine into the synaptic cleft. This acetylcholine then binds to receptors on the muscle cell membrane, initiating muscle contraction by depolarizing the muscle cell membrane and allowing the action potential to propagate along the muscle fiber.
Acetylcholine is the primary neurotransmitter released by motor neurons at the neuromuscular junction to stimulate muscle contraction. It binds to receptors on the muscle cell membrane, initiating a series of events that ultimately lead to muscle contraction.