Fig. 1. The K2P channels in astrocytes. The scheme summarizes the known functions and regulatory mechanisms of K2P channels in astrocytes, and suggests the strategies for future studies. In astrocytes, TWIK1 (green) and TREK1 (blue) are highly expressed and form heterodimeric channels. The TWIK1-TREK1 channel mainly contributes to passive conductance that is a leak K+ background current in astrocytes (blue box). The heterodimeric channel also mediates glutamate release from astrocytes that does not require exocytotic machinery proteins, such as SNARE components. The release process is triggered by a direct interaction between a TREK1 subunit and the Gβγ subunits after the activation of Gαi-protein coupled receptors (orange box). βCOP, PKA, and PKC are already known to control TREK1 by protein-protein interaction or by phosphorylation after GPCR activation in non-astrocytic cells. However, the effector proteins are also expressed in astrocytes, so they may regulate the TWIK1-TREK1 channel by similar mechanisms (gray objects and dashed lines). In addition, other novel interacting partners of the K2P channels that can be novel regulators are expected to be identified in astrocytes in future studies. As suggested by some studies, there is the possibility that other K2P channels, such as TASK1 may be expressed and could contribute to the function of astrocytes (K2P channel in orange).
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