Michaël Russier

The paper shows that 40-Hz firing increases intrinsic excitability in retinal ganglion cells through Cav1-dependent regulation of Kv1 channels, altering their input-output transformation.

This study shows that brief monocular deprivation induces homeostatic changes in intrinsic neuronal excitability in thalamic relay cells, involving Kv1 and Nav1 channel regulation and electrical coupling.

This study shows that reducing external calcium or magnesium ions increases neuronal excitability via CaSR-dependent modulation of Kv1 and Nav1.2 channels.

The paper shows that transient divalent cation depletion induces long-term potentiation of intrinsic neuronal excitability, requiring CaSR, IP3R, and CaMKII.

The paper shows that SST released by O-LM interneurons inhibits neuronal excitability through paracrine and autocrine mechanisms, affecting both synaptic and intrinsic properties.

The paper shows that chronic inactivity does not broadly affect action potentials in neocortical neurons but does in hippocampal neurons under specific conditions.

This study shows that visual activity increases intrinsic excitability in thalamic relay neurons through LTP-IE, involving calcium influx and PKA activation, and links this to visual plasticity and amblyopia.

This study shows that expressing LGI1 in LGI1-deficient neurons restores normal excitability by restoring Kv1.1 channel density and function at the axon initial segment.

The paper uses patient-derived autoantibodies to study LGI1 localization and interactome in mouse brains, revealing its synaptic distribution and novel protein complexes.

This study shows that theta frequency stimulation induces both synaptic and intrinsic long-term potentiation in O-LM interneurons through distinct molecular mechanisms.

This study shows that an epitope-specific LGI1-autoantibody modulates Kv1.1 channel function, increasing neuronal excitability and potentially contributing to epileptiform activity.

The paper shows that endocannabinoid-dependent up-regulation of Kv7 channels mediates long-term depression of intrinsic excitability in O-LM interneurons.

The paper shows axonal sodium channels transmit input synchrony levels to postsynaptic cells by modulating action potential amplitude, enhancing synaptic transmission for synchronous inputs.