Neuron
Volume 84, Issue 4, 19 November 2014, Pages 778-789
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Article
Control and Plasticity of the Presynaptic Action Potential Waveform at Small CNS Nerve Terminals

https://doi.org/10.1016/j.neuron.2014.09.038Get rights and content
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Highlights

  • Presynaptic bouton action potential peaks are constrained by Kv3.1b/Kv1

  • Lower action potential peaks allow large modulation of presynaptic Ca2+ entry

  • Presynaptic action potentials change when Ca2+ channel abundance is altered

  • Expression of this plasticity depends on Kv3.1b/Kv1 function

Summary

The steep dependence of exocytosis on Ca2+ entry at nerve terminals implies that voltage control of both Ca2+ channel opening and the driving force for Ca2+ entry are powerful levers in sculpting synaptic efficacy. Using fast, genetically encoded voltage indicators in dissociated primary neurons, we show that at small nerve terminals K+ channels constrain the peak voltage of the presynaptic action potential (APSYN) to values much lower than those at cell somas. This key APSYN property additionally shows adaptive plasticity: manipulations that increase presynaptic Ca2+ channel abundance and release probability result in a commensurate lowering of the APSYN peak and narrowing of the waveform, while manipulations that decrease presynaptic Ca2+ channel abundance do the opposite. This modulation is eliminated upon blockade of Kv3.1 and Kv1 channels. Our studies thus reveal that adaptive plasticity in the APSYN waveform serves as an important regulator of synaptic function.

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2

Present address: Department of Biology, Dartmouth University, 78 College Street, Room 345, Hanover, NH 03755, USA

3

Present address: Department of Neuroscience, Tufts University School of Medicine, 136 Harrison Avenue, SC203, Boston, MA 02111, USA