Naoki Kogo

This study characterizes a human neuronal model of CACNA1A haploinsufficiency, revealing synaptic deficits and increased intrinsic excitability linked to reduced potassium channel function.

The paper shows that frequency components in EEG signals can arise from retinotopic signal strength variations, not from neural sensitivity to modulated stimuli.

This study investigates SCN1A mutations in excitatory neuronal networks derived from patient hiPSCs, revealing mutation-specific phenotypes that correlate with clinical outcomes and drug responses.

This study shows that SETD1A loss-of-function mutations increase dendritic complexity and neuronal bursting in human neurons via a hyperactive cAMP/PKA pathway, which can be rescued by pharmacological intervention.

The paper compares the dynamics of mutual inhibition between two real neurons with human perceptual competition, finding similar bi-stable behavior under noise and activation changes.