When an action potential reaches the presynaptic neuron, voltage-gated sodium channels open, allowing sodium ions to enter the cell. This influx of sodium triggers the release of neurotransmitters stored in synaptic vesicles into the synaptic cleft. The neurotransmitters then bind to receptors on the postsynaptic neuron, allowing for communication between the two neurons.
Mastitis milk is more alkaline due to the increase in pH caused by the influx of immune cells to the infected mammary gland. The activation of immune defenses in response to infection can lead to the release of alkaline substances, which contribute to the overall alkalinity of the milk.
In the dark, photoreceptor rods are depolarized due to a continuous influx of sodium ions through cGMP-gated channels, maintaining a steady release of glutamate neurotransmitter. This constant release of glutamate signals the dark adaptation state of the photoreceptor.
These communities were called "boomtowns" due to their rapid growth and development, often in response to a sudden economic opportunity such as a gold rush or oil discovery. Boomtowns were characterized by a quick increase in population and infrastructure to support the influx of people seeking their fortunes.
The acid likely disrupted the hydra's osmoregulation process by changing the pH of the water, leading to an influx of water into the hydra's cells. This change in water balance triggered a contraction response in the hydra.
The release of acetylcholine from a synaptic terminal is triggered by the arrival of an action potential at the terminal. This depolarization causes voltage-gated calcium channels to open, leading to an influx of calcium ions into the terminal. The increased calcium levels then trigger the release of acetylcholine vesicles into the synaptic cleft.
Sodium ions
An action potential travels down the neuron and reaches the presynaptic knob. This causes the Calcium ion channels to open and allow an influx of calcium into the knob. The increased concentration of calcium causes the secretory vesicles within the knob to bind to the outer membrane and release their neurotransmitter (e.g. ACh) into the synaptic cleft.
Calcium ions (Ca²⁺) must flow into the presynaptic cell for neurotransmitter release. When an action potential reaches the presynaptic terminal, voltage-gated calcium channels open, allowing Ca²⁺ to enter the cell. This influx of calcium triggers the fusion of neurotransmitter-containing vesicles with the presynaptic membrane, leading to the release of neurotransmitters into the synaptic cleft.
Inhibition of a stimulatory neuron before it synapses, by inhibiting Ca2+ entry and blocking downstream processes, preventing neurotransmitter release, and therefore preventing the neuron generating and EPSP post-synaptically.
When an action potential reaches the end of a neuron's axon, it triggers the release of neurotransmitters from vesicles in the presynaptic terminal into the synaptic cleft. This process is mediated by the influx of calcium ions that enter the neuron during an action potential, causing the vesicles to fuse with the cell membrane and release their contents.
When an action potential arrives at the presynaptic terminal, voltage-gated calcium channels open, allowing calcium ions to enter the cell. The influx of calcium triggers the release of neurotransmitter vesicles from the presynaptic terminal into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, leading to changes in the postsynaptic cell's membrane potential.
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.
Communication across a synapse is initiated by the release of a neurotransmitter from the axon terminal of the presynaptic neuron. When an action potential reaches the axon terminal, it triggers the influx of calcium ions, leading to the fusion of neurotransmitter-containing vesicles with the presynaptic membrane. This process causes the neurotransmitters to be released into the synaptic cleft, where they bind to receptors on the postsynaptic neuron and facilitate communication.
When an action potential reaches the synaptic knob, calcium ions rush into the neuron. This influx of calcium triggers the fusion of synaptic vesicles with the presynaptic membrane, leading to the release of neurotransmitters into the synaptic cleft. The neurotransmitters can then bind to receptors on the postsynaptic neuron, influencing its activity.
Exocytosis. As a result of the influx of Calcium ions, the synaptic vesicles transport the neurotransmitter Ach (Acetylcholine) to the presynaptic membrane, the vesicles fuse to the membrane, and the neurotransmiffer, Ach, diffuses. Once the neurotransmitters cross the synaptic cleft, they bind to the receptors on the post synaptic membrane. Hope it helps a bit.
The action potential moves along the axon and releases neurotransmitters into the synapse.When the presynaptic cell (neuron) fires the action potential, it causes voltage gated sodium ion pores to open at the initial segment of its axon (just after the axon hillock), which allows sodium ions in, which cause adjacent voltage gated sodium ion pores to open, which let in more sodium ions, which do the same thing progressively along the axon, until the action potential reaches the axon terminals, at which point the voltage opens voltage gated calcium ion pores, which cause vesicles (small membrane bounded sacs) full of neurotransmitters to move toward the end of the cell membrane and fuse there, releasing their contents into the synaptic cleft.
Calcium ions trigger the release of neurotransmitter at the presynaptic membrane. When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium ions to enter the cell. The influx of calcium ions triggers the fusion of synaptic vesicles with the presynaptic membrane, leading to the release of neurotransmitter into the synaptic cleft.