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Lee BJ, Yang CH, Lee SY, et al. Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin. Prog Neurobiol. 2021;102182doi: 10.1016/j.pneurobio.2021.102182.
Lee, B. J., Yang, C. H., Lee, S. Y., Lee, S. H., Kim, Y., & Ho, W. K. (2021). Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin. Progress in neurobiology, 102182. https://doi.org/10.1016/j.pneurobio.2021.102182
Lee, Byoung Ju, et al. "Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin." Progress in neurobiology vol. (2021): 102182. doi: https://doi.org/10.1016/j.pneurobio.2021.102182
Lee BJ, Yang CH, Lee SY, Lee SH, Kim Y, Ho WK. Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin. Prog Neurobiol. 2021 Oct 22;102182. doi: 10.1016/j.pneurobio.2021.102182. Epub 2021 Oct 22. PMID: 34695543.
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Prog Neurobiol. 2021 Oct 22;102182. doi: 10.1016/j.pneurobio.2021.102182. Epub 2021 Oct 22.

Voltage-gated calcium channels contribute to spontaneous glutamate release directly via nanodomain coupling or indirectly via calmodulin.

Progress in neurobiology

Byoung Ju Lee, Che Ho Yang, Seung Yeon Lee, Suk-Ho Lee, Yujin Kim, Won-Kyung Ho

Affiliations

  1. Department of Biomedical Sciences, Seoul National University College of Natural Science, Seoul, Republic of Korea; Department of Physiology, Seoul National University College of Natural Science, Seoul, Republic of Korea.
  2. Department of Biomedical Sciences, Seoul National University College of Natural Science, Seoul, Republic of Korea; Department of Physiology, Seoul National University College of Natural Science, Seoul, Republic of Korea; Department of Brain and Cognitive Science, Seoul National University College of Natural Science, Seoul, Republic of Korea.
  3. Department of Biomedical Sciences, Seoul National University College of Natural Science, Seoul, Republic of Korea; Department of Physiology, Seoul National University College of Natural Science, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Republic of Korea; Department of Brain and Cognitive Science, Seoul National University College of Natural Science, Seoul, Republic of Korea.
  4. Department of Physiology, Seoul National University College of Natural Science, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Republic of Korea; Department of Brain and Cognitive Science, Seoul National University College of Natural Science, Seoul, Republic of Korea. Electronic address: [email protected].
  5. Department of Biomedical Sciences, Seoul National University College of Natural Science, Seoul, Republic of Korea; Department of Physiology, Seoul National University College of Natural Science, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Republic of Korea; Department of Brain and Cognitive Science, Seoul National University College of Natural Science, Seoul, Republic of Korea. Electronic address: [email protected].

PMID: 34695543 DOI: 10.1016/j.pneurobio.2021.102182

Abstract

Neurotransmitter release occurs either synchronously with action potentials (evoked release) or spontaneously (spontaneous release). Whether the molecular mechanisms underlying evoked and spontaneous release are identical, especially whether voltage-gated calcium channels (VGCCs) can trigger spontaneous events, is still a matter of debate in glutamatergic synapses. To elucidate this issue, we characterized the VGCC dependence of miniature excitatory postsynaptic currents (mEPSCs) in various synapses with different coupling distances between VGCCs and synaptic vesicles, known as a critical factor in evoked release. We found that most of the extracellular calcium-dependent mEPSCs were attributable to VGCCs in cultured autaptic hippocampal neurons and the mature calyx of Held where VGCCs and vesicles were tightly coupled. Among loosely coupled synapses, mEPSCs were not VGCC-dependent at immature calyx of Held and CA1 pyramidal neuron synapses, whereas VGCCs contribution was significant at CA3 pyramidal neuron synapses. Interestingly, the contribution of VGCCs to spontaneous glutamate release in CA3 pyramidal neurons was abolished by a calmodulin antagonist, calmidazolium. These data suggest that coupling distance between VGCCs and vesicles determines VGCC dependence of spontaneous release at tightly coupled synapses, yet VGCC contribution can be achieved indirectly at loosely coupled synapses.

Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Keywords: Coupling distance; Spontaneous glutamate release; Voltage-gated calcium channels

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