Annie Castonguay

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: An assay for high-throughput screening that led to the identification of KCC2 activators that reduce intracellular chloride concentration rescued K CC2 plasma membrane expression, renormalized stimulus-evoked responses in spinal nociceptive pathways sensitized after nerve injury and alleviated hypersensitivity in a rat model of neuropathic pain.

TL;DR: The findings demonstrate that a peripheral nerve injury causes activated microglia within reward circuitry that result in disruption of dopaminergic signaling and reward behavior, and these results have broad implications that are not restricted to the problem of pain, but are also relevant to affective disorders associated with disruption of reward circuitry.

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 concluded that presynaptic Ca2+ stores act as aCa2+clearance mechanism to limit the duration of transmitter release, whereas Ca2+.