Nicolas Doyon

TL;DR: The findings dissociate morphine-induced hyperalgesia from tolerance and suggest the microglia-to-neuron P2X4-BDNF-KCC2 pathway as a therapeutic target for preventing hyperalGESia without affecting morphine analgesia.

TL;DR: How taking into account dynamical regulation of intracellular Cl(-) is important for understanding how synaptic inhibition fails, how to best detect that failure, why Cl(+) regulation is energetically so expensive, and the overall consequences for therapeutics is discussed.

TL;DR: Recent experimental and theoretical findings concerning the rules of spike timing-dependent inhibitory plasticity and their putative network function are presented.

TL;DR: Results demonstrate that diffusion is crucial for redistributing intracellular Cl− load on a fast time scale, whereas Cl−extrusion controls steady state levels, and uncovers how Cl− regulation depends on a multiplicity of dynamically interacting mechanisms.

TL;DR: It is shown that nerve injury is associated with a reduction in the number of inhibitory synapses in the spinal dorsal horn, accompanied by a BDNF-TrkB-mediated upregulation of synaptic GABAARs and by an α1-to-α2GABAAR subunit switch, providing a mechanistic rationale for the analgesic action of the α2,3 GABAAR benzodiazepine-site ligand L838,417 after nerve injury.