Abstract
MODULATION of transmitter release underlies several forms of learning-related synaptic plasticity, including presynaptic facilitation and long-term potentiation1–4. Although the presynaptic terminals of most neurons are not accessible for direct study, it has often been possible to correlate changes in calcium influx in the cell body, owing to modulation of K+ or Ca2+ channels, with changes in release5–7. Some forms of presynaptic plasticity, however, do not involve changes in Ca2+ influx8–12. Moreover, the presence of multiple types of K+ and Ca2+channels with different subcellular distributions makes the direct measurement of Ca2+ influx into presynaptic terminals essential. Using synapses recon-stituted in culture between Aplysia sensory and motor neurons13, we have imaged Ca2+ influx in presynaptic terminal regions in response to action potentials, and demonstrate that presynaptic facilitation produced by 5-hydroxytryptamine involves enhanced Ca2+ influx through dihydropyridine (DHP)-insensitive Ca2+ channels14 present near release sites. This increased influx is attributable to spike broadening and is significantly correlated with the magnitude of presynaptic facilitation. By contrast, DHP-sensitive channels appear to aid the recovery from depression due to high-frequency stimulation.
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Eliot, L., Kandel, E., Siegelbaum, S. et al. Imaging terminals of Aplysia sensory neurons demonstrates role of enhanced Ca2+ influx in presynaptic facilitation. Nature 361, 634–637 (1993). https://doi.org/10.1038/361634a0
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DOI: https://doi.org/10.1038/361634a0
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