Key result
TREK-1 channel emerges as an attractive therapeutic target modulated by various pharmacological agents.
Why the study?
TREK-1 channel's unique properties and physiological roles suggest it as a promising therapeutic target, warranting a comprehensive review of its characteristics and modulators.
TREK-1 is an attractive therapeutic target due to its distribution in the central nervous system and physiological consequences of its gating.
Supports TREK-1 modulator development for CNS disorders; leaves open clinical translation pending targeted trials.
Potassium (K(+)) channels are membrane proteins expressed in most living cells that selectively control the flow of K(+) ions. More than 80 genes encode the K(+) channel subunits in the human genome. The TWIK-related K(+) channel (TREK-1) belongs to the two-pore domain K(+) channels (K2P) and displays various properties including sensitivity to physical (membrane stretch, acidosis, temperature) and chemical stimuli (signaling lipids, volatile anesthetics). The distribution of TREK-1 in the central nervous system, coupled with the physiological consequences of its opening and closing, leads to the emergence of this channel as an attractive therapeutic target. We review the TREK-1 channel, its structural and functional properties, and the pharmacological agents (agonists and antagonists) able to modulate its gating.
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Vivier et al. (2015) reported a review. TREK-1 channel modulators was evaluated. The TREK-1 channel, due to its distribution in the central nervous system and physiological properties, emerges as an attractive therapeutic target modulated by various pharmacological agents.
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