Axon terminal
Axon terminals (also called synaptic boutons, presynaptic terminals, or end-feet) are distal terminations of the branches of an
Functionally, the axon terminal converts an electrical signal into a chemical signal. When an action potential arrives at an axon terminal (A), neurotransmitter is released and diffuses across the synaptic cleft. If the postsynaptic cell (B) is also a neuron, neurotransmitter receptors generate a small electrical current that changes the postsynaptic potential. If the postsynaptic cell (B) is a muscle cell (neuromuscular junction), it contracts.
Neurotransmitter release
Axon terminals are specialized to release neurotransmitter very rapidly by
Imaging the activity of axon terminals
Historically, calcium-sensitive dyes were the first tool to quantify the calcium influx into synaptic terminals and to investigate the mechanisms of short-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 to construct a genetically encoded sensor that 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
- Calyx of Held, a giant axon terminal in the auditory system
- Neuromuscular junction, axon terminal contacting a muscle cell
- Endocytosis to recycle vesicles after use
- Vesicular monoamine transporter, loading vesicles with neurotransmitter
- Optogenetic methods to measure cellular activity
References
- ^ ISBN 978-1-60535-841-3.
- PMID 6261850.
- PMID 29893445.
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.
- PMID 22026965.
- ISBN 978-1-259-64223-4.
- PMID 11826273.
- S2CID 29102814.
- PMID 23314171.
- PMID 36253353.
Further reading
- 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. PMID 9221772.
- 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. S2CID 53189471.
- 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. S2CID 19618884.
- 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. PMID 3351572.
- 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. S2CID 205056308.