Wataru Inoue

This study identifies recurrent inhibition as a key circuit motif regulating functional states of stress effector neurons through experimental and computational approaches.

The paper identifies a human zona incerta subregion with characteristics of the rodent A13 nucleus using MRI and histology.

This study shows that astrocytic ATRX loss leads to neuronal dysfunction and long-term memory deficits through metabolic and synaptic pathway dysregulation.

The paper compares distractibility between marmosets and macaques in cognitive tasks and links it to dopamine D1 receptor expression in prefrontal parvalbumin neurons.

This study investigates how second-scale neural dynamics in CRH neurons translate stress signals into sustained hormonal outputs, showing firing rate over seconds determines CRH release.

The paper investigates how intrinsic spike frequency adaptation (I-SFA) and inhibitory circuit dynamics contribute to extrinsic-SFA (E-SFA) in primate lateral prefrontal cortex neurons during behavior.

This study investigates how noradrenaline and corticosterone modulate CRH nerve terminal function, finding that noradrenaline inhibits Ca2+ elevations and CRH secretion, while corticosterone suppresses CRH secretion independently of Ca2+ levels.

The paper investigates whether transcriptomic profiles can predict neuronal firing-rate adaptation across brain regions and species using Patch-seq data.

This study shows that deleting ATRX in microglia disrupts chromatin structure, leading to viral mimicry and cognitive deficits in memory tasks.

The paper quantifies microglial contamination in Patch-seq datasets and shows its impact on electrophysiological properties of neurons.

This study identifies a mechanism by which CRH neurons in the hypothalamus switch between activity states in response to stress, using electrophysiology and computational modeling.

This study identifies the hippocampal-hypothalamic circuit as a key pathway for context-dependent innate defensive responses through optogenetic manipulation.

This study shows that chronic activation of hM3Dq in microglia reduces neuroinflammation and sickness behavior in mice by modulating cytokine responses.

The paper shows that repeated stress reduces intrinsic excitability of HPA axis neurons through increased cell size and membrane area, challenging conventional views on excitability plasticity.