synaptic cleft
Acetylcholine is the chemical that transmits signals across the neuromuscular junction. It binds to receptors on the muscle cell membrane, leading to muscle contraction.
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.
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.
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.
Acetylcholine is the chemical that transmits signals across the neuromuscular junction. It binds to receptors on the muscle cell membrane, leading to muscle contraction.
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.
Acetylcholine or aka ACH is the neurotransmitter that is released from the axon terminal to through the neuromuscular junction across the synaptic cleft which binds to the ACH receptors on the end motor plate of the Sarcolema.
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.
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.
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.
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.
Carbon dioxide moves out of the cells from a higher to lower concentration across the cell membrane. Then the CO2 moves through the capillary wall across the diffusion gradient. The diffusion process is repeated at the capillary/alveolar junction.
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).
Acetylcholine released by the motor neuron at the neuromuscular junction changes the permeability of the cell membrane at the motor end plate. The permeability change allows the influx of positive charge, which triggers an action potential. The action potential spreads across the entire surface of the muscle fiber and into the interior via T tubules. The cytoplasmic concentration of calcium ions (released from the sarcoplasmic reticulum) increases, triggering the start of a contraction. The contraction ends when AChE removes the ACh from the synaptic cleft and motor end plat
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. "