Acetylcholine
The axon terminal of a nerve cell is adjacent to the neuromuscular junction. The axon terminal releases neurotransmitters that transmit signals across the synapse to the muscle fiber. This signal triggers muscle contraction.
"Botox" is actually a poison. It prevents muscle movement by preventing the nerve impulse to travel from the neuron across the neuromuscular junction and prevents the muscle from contracting. It is the toxin produced by the microbe that causes botulism.
When an action potential reaches the end of a motor neuron, it triggers the release of neurotransmitters (acetylcholine) into the synaptic cleft. These neurotransmitters bind to receptors on the muscle cell membrane, causing depolarization of the muscle cell and ultimately leading to muscle contraction.
No, depolarization in the heart is not passed cell to cell in the same way as at the neuromuscular junction. In the heart, gap junctions allow for direct electrical coupling between adjacent cardiac muscle cells, allowing the depolarization signal to quickly spread from cell to cell. In the neuromuscular junction, depolarization is transmitted by the release of neurotransmitters across the synaptic cleft from a neuron to a muscle cell.
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.
The axon terminal of a nerve cell is adjacent to the neuromuscular junction. The axon terminal releases neurotransmitters that transmit signals across the synapse to the muscle fiber. This signal triggers muscle contraction.
a chemical that transmits a nervous systems signal across a synapse.
"Botox" is actually a poison. It prevents muscle movement by preventing the nerve impulse to travel from the neuron across the neuromuscular junction and prevents the muscle from contracting. It is the toxin produced by the microbe that causes botulism.
When an action potential reaches the end of a motor neuron, it triggers the release of neurotransmitters (acetylcholine) into the synaptic cleft. These neurotransmitters bind to receptors on the muscle cell membrane, causing depolarization of the muscle cell and ultimately leading to muscle contraction.
No, depolarization in the heart is not passed cell to cell in the same way as at the neuromuscular junction. In the heart, gap junctions allow for direct electrical coupling between adjacent cardiac muscle cells, allowing the depolarization signal to quickly spread from cell to cell. In the neuromuscular junction, depolarization is transmitted by the release of neurotransmitters across the synaptic cleft from a neuron to a muscle cell.
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.
Motor neurons meet the muscle cells at neuromuscular junctions. Neurotransmitters are passed from the nerve across a synaptic cleft to the muscle to make it contract. Any damage to this nerve will mean that those cells will not contract (move).
This is the neuromuscular junction. The action potential travels down the presynaptic motor neuron, releasing acetylcholine (ACh), which cross the synapse (neuromuscular junction), to bind to receptors on the end plate of muscle fibers, which induces depolarization, causing the muscle to contract.
No, the impulse traveling down the axon ends at the axon terminal but causes the axon terminal to release neurotransmitters. The neurotransmitters diffuse across the synaptic cleft causing the sarcolemma of the muscle to initiate its own impulse.
Curare acts by blocking the transmission of nerve impulses at the neuromuscular junction, leading to muscle paralysis. It does this by binding to and blocking nicotinic acetylcholine receptors on the post-synaptic membrane, preventing the action potential from propagating across the muscle cell membrane.
It depends on what the next structure is. If it is another neurone, then it is a synapse. If it is skeletal muscle, then the it is a neuromuscular junction. If it is any other type of muscle, then it is a myoneural junction.
The potential across a pn junction is called potential barrier because majority charge carriers have to overcome this potential before crossing the junction.