The novel structural class of mammalian channels with four transmembrane se
gments and two pore regions comprise background K+ channels (TWIK-1, TREK-1
, TRAAK, TASK, and TASK-2) with unique physiological functions (1-6). Unlik
e its counterparts, TRAAK is only expressed in neuronal tissues, including
brain, spinal cord, and retina (1). This report shows that TRAAK, which was
known to be activated by arachidonic acid (3), is also opened by membrane
stretch. Mechanical activation of TRAAK is induced by a convex curvature of
the plasma membrane and can be mimicked by the amphipathic membrane crenat
or trinitrophenol. Cytoskeletal elements are negative tonic regulators of T
RAAK. Membrane depolarization and membrane cremation synergize with stretch
-induced channel opening. Finally, TRAAK is reversibly blocked by micromola
r concentrations of gadolinium, a well known blocker of stretch-activated c
hannels. Mechanical activation of TRAAK in the central nervous system may p
lay an important role during growth cone motility and neurite elongation.