Kazuhiro Yamakawa

This study uses CRISPR-ON to increase Stxbp1 expression in a mouse model, restoring Munc18-1 protein levels but not fully reversing disease symptoms.

This study shows that reducing Nav1.1 in the dorsal striatum increases hyperthermia-induced seizures more than in the neocortex or nucleus accumbens.

This study shows that reduced excitatory input to the nucleus accumbens due to Scn2a haploinsufficiency impairs sociability without affecting dopamine levels.

The paper examines the co-expression patterns of voltage-gated sodium channel subunits in neurons across different brain regions and developmental stages, revealing distinct subunit combinations in inhibitory and excitatory neurons.

The paper identifies nucleus accumbens parvalbumin-expressing fast-spiking inhibitory neurons as critical for convulsive seizure generation in mice with STXBP1 or SCN2A mutations.

This study identifies myoclonin1's interaction with IP3 receptors and PRKCSH, showing it modulates ER-Ca2+ homeostasis, which may contribute to epilepsy in EFHC1 mutation carriers.

The paper introduces an AI framework to simulate and predict mechanisms of consciousness and disorders, validated with neurophysiological data.

The paper identifies a preserved cross-frequency cortical-thalamic communication channel during conscious states and shows its disruption in unconsciousness and enhancement in psychedelic states.

The paper investigates brain pH and lactate levels in animal models of neuropsychiatric disorders, finding decreased pH and increased lactate levels as common features across multiple models.

The paper confirms mutually exclusive Nav1.1 and Nav1.2 expression in neocortical neurons and identifies Nav1.1 expression in specific excitatory subpopulations.

This study identifies CUX2 and CASP variants in temporal lobe epilepsy patients and shows they increase seizure susceptibility and excitatory synaptic transmission.

The paper investigates cross-modal plasticity in mouse autism models, finding enhanced auditory responses in visual cortex linked to E/I circuit imbalance.