Nicolas Gilbert

This study investigates the role of THIK2 channels in pain regulation through molecular, electrophysiological, and behavioral analyses in knock-out mice, revealing their involvement in limiting neuronal hyperexcitability and suggesting therapeutic potential for chronic pain.

The paper identifies a network of residues responsible for TWIK1 channel's pH-dependent shift in ionic selectivity from K+ to Na+ using MD simulations, mutagenesis, and electrophysiology.