Dominik Oliver

TL;DR: It is reported here that phosphatidylinositol-4, 5-bisphosphate (PIP2) and phosphorus-4-phosphates(PIP) controlled ATP inhibition of cloned KATP channels (Kir6.2 and SUR1) and represents a mechanism for control of excitability through phospholipids.

TL;DR: It is shown that voltage sensitivity is conferred to prestin by the intracellular anions chloride and bicarbonate, which support a model in which anions act as extrinsic voltage sensors, which bind to the prestin molecule and thus trigger the conformational changes required for motility of OHCs.

TL;DR: Heterologously expressed BKCa-Cav complexes reconstitute a functional “Ca2+ nanodomain” where Ca2+ influx through the Cav channel activates BK Ca in the physiological voltage range with submillisecond kinetics, enabling BkCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system.

TL;DR: It is shown that membrane lipids can convert A-type channels into delayed rectifiers and vice versa and that bidirectional control of Kv channel gating by lipids may provide a mechanism for the dynamic regulation of electrical signaling in the nervous system.

TL;DR: It is shown here that unitary inhibitory postsynaptic currents at this synapse are mediated by SK2 channels and occur rapidly, with rise and decay time constants of approximately 6 ms and approximately 30 ms, respectively.