Curare poisoning affects the motor end plate. Curare blocks nicotinic acetylcholine receptors on muscle cells at the neuromuscular junction, preventing the binding of acetylcholine and leading to muscle paralysis.
The receptors found on the end of the motor end plate are called nicotinic acetylcholine receptors. These receptors respond to the neurotransmitter acetylcholine released from the motor neuron and play a crucial role in initiating muscle contraction.
Acetylcholine is the primary neurotransmitter released at the motor end plate, where it binds to receptors on muscle cells to initiate muscle contraction.
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.
The folded region of the sarcolemma at the neuromuscular junction is called the motor end plate. It is responsible for receiving signals from the motor neuron and initiating muscle contraction. The motor end plate is rich in acetylcholine receptors, which play a key role in neurotransmission at the neuromuscular junction.
Motor end plate is a specialized area on a muscle fiber that forms a neuromuscular junction with a motor neuron. It is where the nerve impulse from the motor neuron triggers the muscle fiber to contract. The motor end plate is crucial for muscle function and movement.
The point at which a motor neuron synapses with a muscle fiber's motor end plate is called the neuromuscular junction. This is where the nerve impulse is transmitted from the motor neuron to the muscle fiber, leading to muscle contraction.
Curare poisoning affects the motor end plate. Curare blocks nicotinic acetylcholine receptors on muscle cells at the neuromuscular junction, preventing the binding of acetylcholine and leading to muscle paralysis.
motor end plate
The receptors found on the end of the motor end plate are called nicotinic acetylcholine receptors. These receptors respond to the neurotransmitter acetylcholine released from the motor neuron and play a crucial role in initiating muscle contraction.
Acetylcholine is the primary neurotransmitter released at the motor end plate, where it binds to receptors on muscle cells to initiate muscle contraction.
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.
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The folded region of the sarcolemma at the neuromuscular junction is called the motor end plate. It is responsible for receiving signals from the motor neuron and initiating muscle contraction. The motor end plate is rich in acetylcholine receptors, which play a key role in neurotransmission at the neuromuscular junction.
A deficiency of ACh receptors in a motor end plate would cause muscle weakness or paralysis. This condition is called myasthenia gravis.
Neuromuscular Junction
When acetylcholine binds to receptors at the motor plate, it triggers the opening of ion channels in the muscle membrane. This allows sodium ions to flow into the muscle cell, leading to depolarization of the membrane and initiation of a muscle action potential. Subsequently, this action potential travels along the muscle cell membrane, leading to muscle contraction.