Let's picture a presynaptic neuron, a synaptic cleft, and a postsynaptic neuron.
An action potential reaches the terminal of a presynaptic neurone and triggers an opening of Ca ions enters into the depolarized terminal. This influx of Ca ions causes the presynaptic vesicles to fuse with the presynaptic membrane. This releases the neurotransmitters into the synaptic cleft.
The neurotransmitters diffuse through the synaptic cleft and bind to specific postsynaptic membrane receptors. This binding changes the receptors into a ion channel that allows cations like Na to enter into the postsynaptic neuron. As Na enters the postsynaptic membrane, it begins to depolarize and an action potential is generated.
No, neurotransmitters that depress the resting potential are called inhibitory neurotransmitters. Excitatory neurotransmitters have the opposite effect, causing depolarization and increasing the likelihood of an action potential.
potassium The answer of potassium is dead wrong. Sodium is the electrolyte that flows into the cell to initiate depolarization. Potassium flows into the cell during repolarization.
Opening of these channels leads to depolarization of the motor endplate, which triggers the release of neurotransmitters (such as acetylcholine) from synaptic vesicles. This initiates the muscle contraction process by activating the muscle fibers.
depolarization
Neurotransmitters bind to specific receptors on the postsynaptic neuron, leading to changes in the membrane potential and potentially causing depolarization. If the depolarization reaches a threshold, it triggers the opening of voltage-gated ion channels, allowing sodium ions to flow into the cell, generating an action potential. This electrical signal then propagates along the neuron's axon to transmit information to other neurons.
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.
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.
Neurotransmitters attach to specific proteins called receptors on the cell membrane. These receptors are typically ligand-gated ion channels or G protein-coupled receptors that initiate cellular responses when neurotransmitters bind to them.
d.
On the axon hillock, there is a concentration of sodium channels whose role are to initiate the depolarization and signal transmission allong the axon. Once the all or none threshold is reached, depolarization occurs in a cascade unidirectional along the length of the axon, with potassium channels open just following the sodium-channel mediated depolarization, such that there is no back-propagation of the signal.
When sound waves cause the stereocilia to bend, it opens ion channels in the hair cells, allowing positively charged ions to enter the cell and depolarize it. This depolarization triggers the release of neurotransmitters, sending signals to the brain to interpret the sound.
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.