When acetylcholine (ACh) receptors open, sodium ions (Na+) primarily flow into the postsynaptic membrane. This influx of positively charged sodium ions leads to depolarization, making the inside of the cell more positive. If the depolarization reaches a certain threshold, it can trigger an action potential in the postsynaptic neuron.
A neurotransmitter binds to specific receptors on the postsynaptic membrane of a receiving neuron, leading to the opening of ion channels. This causes an influx of positively charged ions, such as sodium (Na+), which depolarizes the membrane. If the depolarization reaches a certain threshold, it triggers an action potential by opening voltage-gated sodium channels, allowing further sodium influx and propagating the electrical signal along the neuron.
This modification would likely result in a delayed or weakened depolarization of the postsynaptic neuron membrane. As a consequence, the generation of an action potential may be slower or fail to reach the threshold needed to trigger an action potential, leading to impaired signal transmission between neurons.
A neurotransmitter that allows sodium ions to leak into a postsynaptic neuron causes excitatory postsynaptic potentials. The neurotransmitter that is not synthesized in advance and packaged into synaptic vesicles is nitric oxide.
depolarization of the presynaptic membrane due to an arriving action potential
Cell membrane depolarization is caused by the influx of positively charged ions, such as sodium ions, through ion channels in the membrane. This influx of positive charge reduces the voltage difference across the membrane, leading to depolarization.
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.
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.
The greater influx of sodium ions results in membrane depolarization. This is because sodium ions carry a positive charge, which leads to a decrease in the membrane potential towards zero or a positive value.
A neurotransmitter binds to specific receptors on the postsynaptic membrane of a receiving neuron, leading to the opening of ion channels. This causes an influx of positively charged ions, such as sodium (Na+), which depolarizes the membrane. If the depolarization reaches a certain threshold, it triggers an action potential by opening voltage-gated sodium channels, allowing further sodium influx and propagating the electrical signal along the neuron.
The nerve impulse causes the release of acetylcholine from the motor end plate. This causes the depolarization of the membrane of the adjacent muscle cell.
synaptic cleft. This release allows the neurotransmitters to bind to receptors on the postsynaptic neuron, leading to changes in its membrane potential and potentially initiating a new action potential in the receiving neuron.
This modification would likely result in a delayed or weakened depolarization of the postsynaptic neuron membrane. As a consequence, the generation of an action potential may be slower or fail to reach the threshold needed to trigger an action potential, leading to impaired signal transmission between neurons.
A neurotransmitter that allows sodium ions to leak into a postsynaptic neuron causes excitatory postsynaptic potentials. The neurotransmitter that is not synthesized in advance and packaged into synaptic vesicles is nitric oxide.
depolarization of the presynaptic membrane due to an arriving action potential
Cell membrane depolarization is caused by the influx of positively charged ions, such as sodium ions, through ion channels in the membrane. This influx of positive charge reduces the voltage difference across the membrane, leading to depolarization.