Axon terminals(also calledterminal boutons,synaptic boutons,end-feet,orpresynaptic terminals) are distal terminations of the branches of anaxon.An axon, also called a nerve fiber, is a long, slender projection of anerve cellthat conducts electrical impulses calledaction potentialsaway from the neuron'scell bodyto transmit those impulses to other neurons, muscle cells, or glands. Most presynaptic terminals in the central nervous system are formed along the axons (en passant boutons), not at their ends (terminal boutons).
Functionally, the axon terminal converts an electrical signal into a chemical signal. When an action potential arrives at an axon terminal (A),the neurotransmitteris released and diffuses across the synaptic cleft. If the postsynaptic cell (B) is also aneuron,neurotransmitter receptorsgenerate a small electrical current that changes thepostsynaptic potential.If the postsynaptic cell (B) is amuscle cell(neuromuscular junction), it contracts.
Neurotransmitter release
editAxon terminals are specialized to release neurotransmitters very rapidly byexocytosis.[1]Neurotransmitter molecules are packaged intosynaptic vesiclesthat cluster beneath the axon terminal membrane on the presynaptic side (A) of a synapse. Some of these vesicles aredocked,i.e., connected to the membrane by several specialized proteins, such as theSNARE complex.The incomingaction potentialactivatesvoltage-gated calcium channels,leading to an influx of calcium ions into the axon terminal. TheSNARE complexreacts to these calcium ions. It forces the vesicle's membrane to fuse with thepresynaptic membrane,releasing their content into the synaptic cleft within 180μsof calcium entry.[2][3][4]When receptors in the postsynaptic membrane bind this neurotransmitter and openion channels,information is transmitted between neurons (A) and neurons (B).[5]To generate anaction potentialin the postsynaptic neuron, manyexcitatory synapsesmust be active at the same time.[1]
Imaging the activity of axon terminals
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Historically,calcium-sensitive dyeswere the first tool to quantify the calcium influx into synaptic terminals and to investigate the mechanisms ofshort-term plasticity.[6]The process of exocytosis can be visualized with pH-sensitive fluorescent proteins (Synapto-pHluorin): Before release, vesicles are acidic, and the fluorescence is quenched. Upon release, they are neutralized, generating a brief flash of green fluorescence.[7]Another possibility is constructing agenetically encoded sensorthat becomes fluorescent when bound to a specific neurotransmitter, e.g.,glutamate.[8]This method is sensitive enough to detect the fusion of a single transmitter vesicle in brain tissue and to measure the release probability at individual synapses.[9]
See also
edit- Calyx of Held,a giant axon terminal in theauditory system
- Neuromuscular junction,axon terminal contacting a muscle cell
- Endocytosisto recycle vesicles after use
- Vesicular monoamine transporter,loading vesicles with neurotransmitter.
- Optogenetic methods to measure cellular activity
References
edit- ^abPurves, Dale; Augustine, George J.; Fitzpatrick, David, eds. (2019).Neuroscience(6th ed.). New York: Sinauer Associates / Oxford University Press.ISBN978-1-60535-841-3.
- ^Llinás R, Steinberg IZ, Walton K (March 1981)."Relationship between presynaptic calcium current and postsynaptic potential in squid giant synapse".Biophysical Journal.33(3):323–351.Bibcode:1981BpJ....33..323L.doi:10.1016/S0006-3495(81)84899-0.PMC1327434.PMID6261850.
- ^Rizo J (August 2018)."Mechanism of neurotransmitter release coming into focus".Protein Science(Review).27(8):1364–1391.doi:10.1002/pro.3445.PMC6153415.PMID29893445.
Research for three decades and major recent advances have provided crucial insights into how neurotransmitters are released by Ca2+ -triggered synaptic vesicle exocytosis, leading to reconstitution of basic steps that underlie Ca2+ -dependent membrane fusion and yielding a model that assigns defined functions for central components of the release machinery.
- ^Südhof TC, Rizo J (December 2011)."Synaptic vesicle exocytosis".Cold Spring Harbor Perspectives in Biology.3(12): a005637.doi:10.1101/cshperspect.a005637.PMC3225952.PMID22026965.
- ^Siegelbaum, Steven A. (2021). Kandel, Eric R.; Koester, John D.; Mack, Sarah H. (eds.).Principles of neural science(6th ed.). New York: McGraw-Hill.ISBN978-1-259-64223-4.
- ^Zucker RS, Regehr WG (2002). "Short-term synaptic plasticity".Annual Review of Physiology.64(1):355–405.doi:10.1146/annurev.physiol.64.092501.114547.PMID11826273.
- ^Burrone J, Li Z, Murthy VN (2006). "Studying vesicle cycling in presynaptic terminals using the genetically encoded probe synaptopHluorin".Nature Protocols.1(6):2970–2978.doi:10.1038/nprot.2006.449.PMID17406557.S2CID29102814.
- ^Marvin JS, Borghuis BG, Tian L, Cichon J, Harnett MT, Akerboom J, et al. (February 2013)."An optimized fluorescent probe for visualizing glutamate neurotransmission".Nature Methods.10(2):162–170.doi:10.1038/nmeth.2333.PMC4469972.PMID23314171.
- ^Dürst CD, Wiegert JS, Schulze C, Helassa N, Török K, Oertner TG (October 2022)."Vesicular release probability sets the strength of individual Schaffer collateral synapses".Nature Communications.13(1): 6126.doi:10.1038/s41467-022-33565-6.PMC9576736.PMID36253353.
Further reading
edit- Cragg SJ, Greenfield SA (August 1997)."Differential autoreceptor control of somatodendritic and axon terminal dopamine release in substantia nigra, ventral tegmental area, and striatum".The Journal of Neuroscience.17(15):5738–5746.doi:10.1523/JNEUROSCI.17-15-05738.1997.PMC6573186.PMID9221772.
- Vaquero CF, de la Villa P (October 1999). "Localisation of the GABA(C) receptors at the axon terminal of the rod bipolar cells of the mouse retina".Neuroscience Research.35(1):1–7.doi:10.1016/S0168-0102(99)00050-4.PMID10555158.S2CID53189471.
- Roffler-Tarlov S, Beart PM, O'Gorman S, Sidman RL (May 1979). "Neurochemical and morphological consequences of axon terminal degeneration in cerebellar deep nuclei of mice with inherited Purkinje cell degeneration".Brain Research.168(1):75–95.doi:10.1016/0006-8993(79)90129-X.PMID455087.S2CID19618884.
- Yagi T, Kaneko A (February 1988). "The axon terminal of goldfish retinal horizontal cells: a low membrane conductance measured in solitary preparations and its implication to the signal conduction from the soma".Journal of Neurophysiology.59(2):482–494.doi:10.1152/jn.1988.59.2.482.PMID3351572.
- LTP promotes formation of multiple spine synapses between a single axon terminal and a dendrite.Toni N, Buchs PA, Nikonenko I, Bron CR, Muller D (November 1999). "LTP promotes formation of multiple spine synapses between a single axon terminal and a dendrite".Nature.402(6760):421–425.Bibcode:1999Natur.402..421T.doi:10.1038/46574.PMID10586883.S2CID205056308.