Frédéric Brocard

The paper identifies SK2/3 channels coupled with T-type Ca2+ channels as a mechanism gating spinal locomotor rhythm generation, showing their role in initiating and terminating locomotor activity.

The paper investigates ionic mechanisms underlying bistability in spinal motoneurons using a computational model and mouse recordings, identifying key currents involved in plateau potentials and bistable firing.

This study shows that enhancing astrocytic Kir4.1 function reduces spasticity in SCI mice by improving K+ uptake and preventing neuronal hyperexcitability.

This study investigates how motoneuron size relates to bistability in mouse spinal motoneurons, finding that larger neurons exhibit higher bistability due to specific ionic currents.

This study identifies Nav1.6 as the primary channel mediating persistent sodium current in spinal motoneurons and shows its role in locomotion and posture through nonlinear dynamics.

This study identifies astrocytic Kir4.1 channels as critical for neuronal rhythmicity in the spinal CPG, showing their role in regulating locomotion through K+ clearance.

The paper investigates hiPSC-derived motor neurons with VRK1 mutations, finding altered action potential waveforms and shorter axonal initial segments, suggesting a link to motor neuron disease.

The paper identifies a persistent potassium current (IM) that interacts with the persistent sodium current (INaP) to regulate locomotion speed in neonatal rodents.