When the neurotransmitter acetylcholine binds to the motor end plate, it triggers the opening of sodium channels in the muscle cell membrane. This influx of sodium ions leads to depolarization of the cell, creating an action potential that propagates along the muscle fiber, ultimately leading to muscle contraction.
Potassium efflux is controlled by voltage-gated potassium channels, while sodium influx is controlled by voltage-gated sodium channels. These channels open and close in response to changes in membrane potential, regulating the flow of ions in and out of the cell.
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 influx of sodium ions causes depolarization of the cell membrane, making the interior less negative. This depolarization can trigger the opening of voltage-gated ion channels, leading to the propagation of an action potential. Sodium-potassium pumps work to restore the original ion concentrations, repolarizing the cell.
The combining of the neurotransmitter with the muscle membrane receptors causes the membrane to become permeable to sodium ions and depolarization of the membrane. This depolarization triggers an action potential that leads to muscle contraction.
depolarization.
Binding of acetylcholine to nicotinic acetylcholine receptors opens ion channels that allow both sodium and potassium ions to permeate the membrane. This causes depolarization of the membrane potential, leading to an excitatory response in the cell.
The opening of voltage-gated sodium channels in response to a stimulus. Sodium ions flow into the cell, causing depolarization as the inside becomes more positively charged.
The first step for nerve impulse generation is the depolarization of the cell membrane, which is triggered by a stimulus. This depolarization causes a change in the electrical charge of the cell membrane, leading to the opening of ion channels and the initiation of an action potential.
it prevents sodium channels from opening which removes a neuron's resting membrane potential
A nerve generates an action potential through a series of events involving the opening and closing of ion channels. Initially, a stimulus causes sodium channels to open, allowing an influx of sodium ions, depolarizing the cell membrane. This triggers the opening of voltage-gated sodium channels, leading to a rapid depolarization phase and the propagation of the action potential along the nerve.
Local depolarization is caused by the opening of voltage-gated sodium channels in response to the binding of neurotransmitters or other stimuli. This influx of sodium ions results in membrane depolarization, reaching the threshold potential needed to generate an action potential.
When voltage-gated sodium channels open, sodium ions rush into the neuron, causing depolarization. This depolarization spreads along the axon due to local currents, triggering the opening of sodium channels in adjacent regions, leading to further depolarization and propagation of the action potential down the axon. Meanwhile, voltage-gated potassium channels open, allowing potassium to flow out of the cell, contributing to repolarization and restoring the neuron's resting potential.
When a nerve impulse is conducted, the neuronal cell membrane undergoes changes in electrical potential. This starts with a rapid influx of sodium ions into the cell through voltage-gated sodium channels, depolarizing the membrane. This depolarization triggers the opening of adjacent sodium channels, resulting in an action potential that travels along the membrane. After the impulse passes, the sodium channels close, and potassium channels open, allowing potassium ions to exit the cell and restore the resting potential.
The binding of neurotransmitters to receptors on the muscle membrane triggers the opening of ion channels, allowing sodium ions to enter the muscle cell. This influx of sodium ions initiates an action potential, leading to muscle contraction.
During depolarization, the neuron's membrane potential becomes less negative as positive ions enter the cell. This is due to the opening of voltage-gated sodium channels, allowing sodium ions to flow into the cell.
When the neurotransmitter acetylcholine binds to the motor end plate, it triggers the opening of sodium channels in the muscle cell membrane. This influx of sodium ions leads to depolarization of the cell, creating an action potential that propagates along the muscle fiber, ultimately leading to muscle contraction.