Antoine G. Godin

This study shows that BDNF-TrkB and NMDAR signaling pathways synergistically regulate KCC2 function, trafficking, and degradation through distinct Ca2+-dependent mechanisms.

The paper investigates how sensory fibers encode thermal and mechanical nociceptive input in mice, finding that modality separation dominates in the innocuous range while polymodality predominates in the noxious range.

The paper shows that EMMPRIN activation in astrocytes contributes to their pathological phenotype in ALS and suggests anti-EMMPRIN antibodies as a potential therapeutic approach.

This study identifies KCC2 as an early biomarker and therapeutic target for ALS by showing its downregulation in motor neurons and the ability of KCC2-enhancing compounds to delay disease progression.

The paper identifies a sex-specific neuronal mechanism of spinal hyperexcitability in pain models, showing differences in BDNF signaling between male and female rodents and humans.

The paper develops an in silico model of trans-synaptic nanocolumns to study their impact on synaptic current and shows they reinforce weak synapses when presynaptic vesicles contain few neurotransmitters.