Basically, the release of neurotransmitters into a synaptic cleft, from an axon terminal, by causing the vesicles containing the neurotransmitters to fuse with the cell membrane, spilling their contents into the synapse.
a previous answer:
It can also play parts in several receptor mediated effects, these are too vast to mention them all.
Search "G-Protein coupled receptors and IP3 signal cascades" in Google. Might explain more.
They let calcium ions in, which cause neurotransmitters to be released into a synapse, which cause a neural impulse to flow down a dendrite toward the axon hillock, where the action potential is generated. In more detail: The first steps occur in an axon terminal, which is where the calcium channels are located. When calcium channels are caused to open by the arrival of an action potential at an axon terminal, calcium ions enter the axon terminal, where the calcium ions bind to vesicles containing neurotransmitters, which causes the vesicles to fuse to the cell membrane, forming an opening through which the neurotransmitters are released into the synaptic cleft. The neurotransmitters diffuse quickly across the synaptic cleft (the gap between two neurons), where they fit into receptors on the surface of the postsynaptic neuron, usually on a dendrite or a dendritic spine, and cause ligand-gated sodium ion pores to open, allowing sodium ions into the postsynaptic neuron, which causes an electrotonic impulse to travel down a dendrite, across the soma, to the axon hillock, where the impulses are summed up, and if a sufficient voltage potential is realized, an action potential is initiated in the initial segment of the axon.
No, subthreshold stimulation is not sufficient to trigger an action potential. The membrane potential needs to reach a certain threshold level for an action potential to be generated. Subthreshold stimulation only produces graded potentials that do not reach the threshold for firing an action potential.
Calcium ions cause the neurotransmitter vesicles to fuse with the axon terminal. When an action potential reaches the axon terminal, voltage-gated calcium ion pores are opened, allowing calcium ions into the axon terminal. These ions initiate the release of neurotransmitter vesicles stored on elements of the cytoskeleton located near the presynaptic membrane; they then travel to the presynaptic membrane, where they first dock, and then fuse with the presynaptic membrane, forming an opening or pore through which the neurotransmitters are released into the synaptic cleft.
The voltage-gated Na+ channels get deactivated, thus the sodium ions cannot diffuse into the cell and cause depolarisation and this also provides time for the membrane to prepare for its second action potential.
No, it doesn't become "larger" - the peak potential is always the same - it is a digital signal. Stronger stimulus will cause the nerve cell to fire more often - therefore stimulus strength is translated as action potential frequency.
When Ach enters the synaptic cleft (gap) it open chemically gated sodium channels that starts an action potential spreading through the sarcolemma of the myofibril. This action potential spreads down the T-tubules and "shocks" the sarcoplasmic reticulum into releasing calcium ions.
They let calcium ions in, which cause neurotransmitters to be released into a synapse, which cause a neural impulse to flow down a dendrite toward the axon hillock, where the action potential is generated. In more detail: The first steps occur in an axon terminal, which is where the calcium channels are located. When calcium channels are caused to open by the arrival of an action potential at an axon terminal, calcium ions enter the axon terminal, where the calcium ions bind to vesicles containing neurotransmitters, which causes the vesicles to fuse to the cell membrane, forming an opening through which the neurotransmitters are released into the synaptic cleft. The neurotransmitters diffuse quickly across the synaptic cleft (the gap between two neurons), where they fit into receptors on the surface of the postsynaptic neuron, usually on a dendrite or a dendritic spine, and cause ligand-gated sodium ion pores to open, allowing sodium ions into the postsynaptic neuron, which causes an electrotonic impulse to travel down a dendrite, across the soma, to the axon hillock, where the impulses are summed up, and if a sufficient voltage potential is realized, an action potential is initiated in the initial segment of the axon.
Yes, you see when a action potential process is taking place the negative ions are in the center of the nerve and the positives are on the outside, during the action potential however they swap places, which in doing so changes the electrical and chemicals in the nerve cell.
In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane.
The ion that enters the axon nerve terminal to trigger neurotransmitter release is calcium (Ca2+). When an action potential reaches the nerve terminal, voltage-gated calcium channels open, allowing calcium ions to flow into the cell and initiate the process of exocytosis of neurotransmitter-containing vesicles.
A synapse and an action potential have a flip-flopping cause and effect relationship, in that an action potential in a presynaptic neuron initiates a release of neurotransmitters across a synapse, which can then subsequently potentially trigger an action potential in the axon of the postsynaptic neuron, which would then cause release of neurotransmitters across a following synapse.
No, subthreshold stimulation is not sufficient to trigger an action potential. The membrane potential needs to reach a certain threshold level for an action potential to be generated. Subthreshold stimulation only produces graded potentials that do not reach the threshold for firing an action potential.
Calcium ions cause the neurotransmitter vesicles to fuse with the axon terminal. When an action potential reaches the axon terminal, voltage-gated calcium ion pores are opened, allowing calcium ions into the axon terminal. These ions initiate the release of neurotransmitter vesicles stored on elements of the cytoskeleton located near the presynaptic membrane; they then travel to the presynaptic membrane, where they first dock, and then fuse with the presynaptic membrane, forming an opening or pore through which the neurotransmitters are released into the synaptic cleft.
The voltage-gated Na+ channels get deactivated, thus the sodium ions cannot diffuse into the cell and cause depolarisation and this also provides time for the membrane to prepare for its second action potential.
Citrate can cause hypocalcemia because it binds to calcium ions in the bloodstream, forming a complex that reduces the amount of free, ionized calcium available for physiological functions. This effect is particularly notable during blood transfusions, where citrate is used as an anticoagulant. As citrate is metabolized by the liver, the calcium levels may return to normal, but during the period of binding, hypocalcemia can occur, leading to potential symptoms such as muscle spasms or cardiac issues.
No, it doesn't become "larger" - the peak potential is always the same - it is a digital signal. Stronger stimulus will cause the nerve cell to fire more often - therefore stimulus strength is translated as action potential frequency.
Not all stimuli generate an action potential because an action potential occurs only when a stimulus reaches a certain threshold level of depolarization in a neuron. Sub-threshold stimuli may cause local changes in membrane potential but are not strong enough to trigger the rapid depolarization needed for an action potential. Additionally, the neuron has a refractory period during which it cannot fire another action potential, further ensuring that only sufficiently strong stimuli result in this electrical signal. This selective response allows the nervous system to filter and prioritize important information.