Three residues work together as a valve-like mechanism to control desensitization from pre-open and open states in the ion channels ASIC1a, ASIC2a, and ASIC3.

The Drosophila equivalent of Substance P signaling modulates nociceptive sensitization by regulating Hedgehog signaling within nociceptive sensory neurons.

Cell cycle gating enables a temporal compartmentalization of negative vs positive feedback control processes, leading to differential responses to repetitive interferon stimulations.

Phosphatidylglycerol binding at multiple sites stabilizes the open state relative to the desensitized state of a pentameric ligand-gated ion channel.

Differential, state-dependent occupancy of three discrete binding sites on α₁β₃ GABA_A receptors determines whether a specific neurosteroid analogue potentiates or inhibits GABA-elicited currents or competitively antagonizes neurosteroid action.

The rotation of the β11-12 linker is a crucial control point for acid-sensing ion channel gating and motion of this linker is required for the channel to desensitize.

Serine and threonine phosphorylation sites work in concert to provide rapid and reproducible desensitization of the G-protein coupled receptor rhodopsin.

The loss of calcium-dependent D2 autoreceptor desensitization caused by prior in vivo cocaine exposure may be conferred by an unexpected role of the D2L splice variant as an autoreceptor.

Desensitization of the D2 autoreceptor is reduced following in vivo cocaine exposure due to plasticity in the D2S and not the D2L splice variant.

The role of C-terminal phosphorylation is critical for the expression of acute desensitization, trafficking and long-term tolerance to morphine.