Neurotransmitters are released from presynaptic neurons through a process known as exocytosis. In this process, neurotransmitters are packaged in small membrane-bound vesicles within the presynaptic neuron and released into the synaptic cleft when an action potential is triggered. This causes the vesicles to fuse with the presynaptic membrane, allowing the neurotransmitter to diffuse across the synaptic cleft and bind to postsynaptic receptors.
neurotransmission (Latin: streaming “passage, crossing” of transmitter “send, let through”) is the process by which signaling molecules called neurotransmitters are released by axon terminal on one neuron (the presynaptic neuron), bind and react with the receivers at the dendrites from another neuron (the postsynaptic neuron) a short distance away. A similar process takes place in retrograde neurotransmissionwhere the dendrites of the postsynaptic neuron release retrograde neurotransmitters (e.g., endocannabinoids; synthesized in response to an increase intracellular calcium levels) that signal through receptors that are located in the axon terminal of the presynaptic neuron, mainly in GABAergic and glutamatergic synapses.
Neurotransmission is regulated by several different factors: the availability and rate of neurotransmitter synthesis, the release of that neurotransmitter, the basal activity of the postsynaptic cell, the number of postsynaptic receptors available for the neurotransmitter to bind to, and the subsequent removal. or deactivation of the neurotransmitter by enzymes or presynaptic reuptake.
In response to a limit action potential or graded electric potentiala neurotransmitter is released in the presynaptic terminal. The released neurotransmitter can then move across the synapse to be detected and bind to receptors on the postsynaptic neuron. Binding of neurotransmitters can influence the postsynaptic neuron in a inhibitory or excitatory manner. The binding of neurotransmitters to receptors on the postsynaptic neuron can trigger short-term changes, such as changes in the membrane potential called postsynaptic potentialsor long-term changes by activation of signal waterfalls.
Neurons form complex biological neural networks through which nerve impulses (action potentials) travel. Neurons do not touch (except in the case of a electrical synapse Through a gap junction); instead, neurons interact at close contact points called synapses. A neuron carries its information through an action potential. When the nerve impulse arrives at the synapse, it can cause the release of neurotransmitters, which influence another (postsynaptic) neuron. The postsynaptic neuron can receive input from many additional neurons, both excitatory and inhibitory. Excitatory and inhibitory influences add up, and if the net effect is inhibitory, the neuron is less likely to “fire” (that is, generate an action potential), and if the net effect is excitatory, the neuron is more likely to shoot. fire. The probability that a neuron will fire depends on how far away it is. membrane potential It’s from threshold potentialthe voltage at which an action potential fires because there is a lot of voltage dependent voltage sodium channels are activated so that the net internal current of sodium exceeds all external currents. Excitatory inputs bring a neuron closer to threshold, while inhibitory inputs bring the neuron closer to threshold. An action potential is an “all or nothing” event; neurons whose membranes have not reached the threshold will not fire, while those that do should fire. Once the action potential is initiated (traditionally in the axon hill), it will propagate along the axon, leading to the release of neurotransmitters in the synaptic button to pass information to another adjacent neuron.
Stages in neurotransmission at the synapse
- Neurotransmitter synthesis. This can occur in cell bodyin the axon or axon terminal.
- Neurotransmitter storage in granules or storage vesicles in the axon terminal.
- Calcium enters the axon terminal during an action potential, causing release of the neurotransmitter in the synaptic cleft.
- After its release, the transmitter binds and activates a receptor on the postsynaptic membrane.
- Neurotransmitter deactivation. The neurotransmitter is either destroyed enzymatically or taken back to the terminal it came from, where it can be reused or degraded and removed.
Neurotransmitters are spontaneously packaged into vesicles and released in individual packets of quanta, regardless of presynaptic action potentials. This slow release is detectable and produces microinhibitory or microexcitatory effects in the postsynaptic neuron. An action potential briefly amplifies this process. Neurotransmitters containing vesicles cluster around active sites and, after being released, can be recycled by one of three proposed mechanisms. The first proposed mechanism involves partial opening and re-closing of the vesicle. The second two involve complete fusion of the vesicle with the membrane, followed by recycling or recycling in the endosome. Vesicular fusion is largely driven by calcium concentration in microdomains located near calcium channels, allowing only microseconds of neurotransmitter release, whereas the return to normal calcium concentration takes a few hundred microseconds. Vesicle exocytosis is thought to be driven by a protein complex called LINKthis is the target for botulinum toxins. Once released, a neurotransmitter enters the synapse and finds the receptors. Neurotransmitter receptors can be ionotropic or g-protein coupled. Ionotropic receptors allow the passage of ions when agonized by a ligand. The main model involves a receptor composed of multiple subunits that allow the coordination of ionic preference. G protein-coupled receptors, also called metabotropic receptors, when bound to a ligand undergo conformational changes resulting in an intracellular response. Termination of neurotransmitter activity is usually done by a transporter, but enzymatic deactivation is also plausible.
Each neuron connects with several other neurons, receiving numerous impulses from them.
sum is the sum of these impulses in the protrusion of the axon. If the neuron receives only excitatory impulses, it will generate an action potential. If, instead, the neuron receives as many inhibitory as excitatory impulses, the inhibition cancels out the excitation and the nerve impulse stops there. Action potential generation is proportional to the probability and pattern of neurotransmitter release and postsynaptic receptor sensitization.
spatial sum means that the effects of impulses received at different locations in the neuron add up, so that the neuron can fire when such impulses are received simultaneously, even if each impulse alone is not sufficient to cause the firing.
time sum means that the effects of impulses received at the same location can add up if the impulses are received in close temporal succession. Thus, the neuron can fire when multiple impulses are received, even though each impulse alone is not enough to cause the firing.
convergence and divergence
Neurotransmission implies both a convergence and a divergence of information. First, one neuron is influenced by many others, resulting in input convergence. When the neuron fires, the signal is sent to many other neurons, resulting in an output divergence. Many other neurons are influenced by this neuron.
Cotransmission is the release of several types of neurotransmitters from a single nerve ending.
At the nerve terminal, neurotransmitters are present within 35- to 50-nm membrane-enclosed vesicles called synaptic vesicles. To release neurotransmitters, synaptic vesicles dock and fuse temporarily at the base of specialized 10- to 15-nm cup-shaped cells. lipoprotein structures on the presynaptic membrane called porosomes. The neuronal porosome proteome was resolved, providing the molecular architecture and complete makeup of the machinery.
Recent studies in a myriad of systems have shown that most, if not all, neurons release a number of different chemical messengers. Cotransmission allows for more complex effects in postsynaptic receptorsand thus allows more complex communication to occur between neurons.
Some neurons can release at least two neurotransmitters at the same time, the other being a cotransmitter, in order to provide the stabilizing negative feedback needed for meaningful encoding in the absence of inhibitory inhibition. interneurons. Examples include:
- GABA–glycine co-release.
- dopamine–glutamate co-release.
- acetylcholine (Ach)-glutamate co-release.
- ACh–vasoactive intestinal peptide (VIP) co-launch.
- ACh–calcitonin gene-related peptide (CGRP) co-release.
- Glutamate–dynorphin co-release (on hippocampus).
noradrenaline and ATP it is kind cotransmitters. It was discovered that the endocannabinoid anadamide and the cannabinoid WIN 55.212-2 may modify the global response to sympathetic nerve stimulation and indicate that prejunctional CB1 receptors mediate the kind– inhibitory action. Thus, cannabinoids can inhibit both noradrenergic and purinergic components of sympathetic neurotransmission.
An unusual pair of cotransmitters is GABA and glutamate, which are released from the same axon terminals of neurons originating in the brain. ventral tegmental area (VTA), internal globus pallidusand supramamillary nucleus. The first two project for the habenula Whereas supramamillary nucleus projections are known to reach the dentate gyrus from the hippocampus.
Neurotransmission is genetically associated with other traits or resources. For example, enrichment analyzes of different signaling pathways led to the discovery of a genetic association with intracranial volume.
- Biological neuron model § Synaptic transmission
- G protein-coupled receptor
- molecular neuropharmacology
- neuromuscular transmission
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