Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023:33:305-331.
doi: 10.1007/978-3-031-34229-5_12.

Regulation of Neurotransmitter Release by K+ Channels

Affiliations

Regulation of Neurotransmitter Release by K+ Channels

Zhao-Wen Wang et al. Adv Neurobiol. 2023.

Abstract

K+ channels play potent roles in the process of neurotransmitter release by influencing the action potential waveform and modulating neuronal excitability and release probability. These diverse effects of K+ channel activation are ensured by the wide variety of K+ channel genes and their differential expression in different cell types. Accordingly, a variety of K+ channels have been implicated in regulating neurotransmitter release, including the Ca2+- and voltage-gated K+ channel Slo1 (also known as BK channel), voltage-gated K+ channels of the Kv3 (Shaw-type), Kv1 (Shaker-type), and Kv7 (KCNQ) families, G-protein-gated inwardly rectifying K+ (GIRK) channels, and SLO-2 (a Ca2+-. Cl-, and voltage-gated K+ channel in C. elegans). These channels vary in their expression patterns, subcellular localization, and biophysical properties. Their roles in neurotransmitter release may also vary depending on the synapse and physiological or experimental conditions. This chapter summarizes key findings about the roles of K+ channels in regulating neurotransmitter release.

Keywords: BK channel; G-protein-gated inwardly rectifying K+ channel; GIRK; KCNQ; Kv1; Kv3; Kv7; Neurotransmitter release; SLO-1; SLO-2; Slo1.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Schneggenburger R, Neher E. Intracellular calcium dependence of transmitter release rates at a fast central synapse. Nature. 2000;406:889–93. https://doi.org/10.1038/35022702 . - DOI - PubMed
    1. Heidelberger R, Heinemann C, Neher E, Matthews G. Calcium dependence of the rate of exocytosis in a synaptic terminal. Nature. 1994;371:513–5. https://doi.org/10.1038/371513a0 . - DOI - PubMed
    1. Lando L, Zucker RS. Ca2+ cooperativity in neurosecretion measured using photolabile Ca2+ chelators. J Neurophysiol. 1994;72:825–30. https://doi.org/10.1152/jn.1994.72.2.825 . - DOI - PubMed
    1. Bollmann JH, Sakmann B, Borst JG. Calcium sensitivity of glutamate release in a calyx-type terminal. Science. 2000;289:953–7. https://doi.org/10.1126/science.289.5481.953 . - DOI - PubMed
    1. Dodson PD, Forsythe ID. Presynaptic K+ channels: electrifying regulators of synaptic terminal excitability. Trends Neurosci. 2004;27:210–7. https://doi.org/10.1016/j.tins.2004.02.012 . - DOI - PubMed

Substances

LinkOut - more resources