Dataset Information

Ca²⁺-Sensitive Potassium Channels.

ABSTRACT: The Ca²⁺ ion is used ubiquitously as an intracellular signaling molecule due to its high external and low internal concentration. Many Ca²⁺-sensing ion channel proteins have evolved to receive and propagate Ca²⁺ signals. Among them are the Ca²⁺-activated potassium channels, a large family of potassium channels activated by rises in cytosolic calcium in response to Ca²⁺ influx via Ca²⁺-permeable channels that open during the action potential or Ca²⁺ release from the endoplasmic reticulum. The Ca²⁺ sensitivity of these channels allows internal Ca²⁺ to regulate the electrical activity of the cell membrane. Activating these potassium channels controls many physiological processes, from the firing properties of neurons to the control of transmitter release. This review will discuss what is understood about the Ca²⁺ sensitivity of the two best-studied groups of Ca²⁺-sensitive potassium channels: large-conductance Ca²⁺-activated K⁺ channels, K_Ca1.1, and small/intermediate-conductance Ca²⁺-activated K⁺ channels, K_Ca2.x/K_Ca3.1.

SUBMITTER: Orfali R

PROVIDER: S-EPMC9861210 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature

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Ca2+-Sensitive Potassium Channels.

Orfali Razan R Albanyan Nora N

Molecules (Basel, Switzerland) 20230116 2

The Ca2+ ion is used ubiquitously as an intracellular signaling molecule due to its high external and low internal concentration. Many Ca2+-sensing ion channel proteins have evolved to receive and propagate Ca2+ signals. Among them are the Ca2+-activated potassium channels, a large family of potassium channels activated by rises in cytosolic calcium in response to Ca2+ influx via Ca2+-permeable channels that open during the action ...[more]

PMID: 36677942

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Project description:Stac protein (named for its SH3- and cysteine-rich domains) was first identified in brain 20 years ago and is currently known to have three isoforms. Stac2, Stac1, and Stac3 transcripts are found at high, modest, and very low levels, respectively, in the cerebellum and forebrain, but their neuronal functions have been little investigated. Here, we tested the effects of Stac proteins on neuronal, high-voltage-activated Ca2+ channels. Overexpression of the three Stac isoforms eliminated Ca2+-dependent inactivation (CDI) of l-type current in rat neonatal hippocampal neurons (sex unknown), but not CDI of non-l-type current. Using heterologous expression in tsA201 cells (together with β and α2-δ1 auxiliary subunits), we found that CDI for CaV1.2 and CaV1.3 (the predominant, neuronal l-type Ca2+ channels) was suppressed by all three Stac isoforms, whereas CDI for the P/Q channel, CaV2.1, was not. For CaV1.2, the inhibition of CDI by the Stac proteins appeared to involve their direct interaction with the channel's C terminus. Within the Stac proteins, a weakly conserved segment containing ∼100 residues and linking the structurally conserved PKC C1 and SH3_1 domains was sufficient to fully suppress CDI. The presence of CDI for l-type current in control neonatal neurons raised the possibility that endogenous Stac levels are low in these neurons and Western blotting indicated that the expression of Stac2 was substantially increased in adult forebrain and cerebellum compared with neonate. Together, our results indicate that one likely function of neuronal Stac proteins is to tune Ca2+ entry via neuronal l-type channels.SIGNIFICANCE STATEMENT Stac protein, first identified 20 years ago in brain, has recently been found to be essential for proper trafficking and function of the skeletal muscle l-type Ca2+ channel and is the site of mutations causing a severe, inherited human myopathy. In neurons, however, functions for Stac protein have remained unexplored. Here, we report that one likely function of neuronal Stac proteins is tuning Ca2+ entry via l-type, but not that via non-l-type, Ca2+ channels. Moreover, there is a large postnatal increase in protein levels of the major neuronal isoform (Stac2) in forebrain and cerebellum, which could provide developmental regulation of l-type channel Ca2+ signaling in these brain regions.

Dataset Information

Ca²⁺-Sensitive Potassium Channels.

Publications

Ca<sup>2+</sup>-Sensitive Potassium Channels.

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