京都大学 · 神経科学
Nagayasu教授の研究室は、セロトニンニューロンの機能とその神経回路機構に注目し、うつ病の病態と治療の神経基盤を解明することを目的としています。特に、背縫線核（DRN）のセロトニンニューロンが報酬と嫌悪のバランスを制御するメカニズムや、陽性記憶に関連する神経集合への選択的活性化を解明しています。また、抗うつ薬の作用メカニズムとして、持続的投与によるセロトニン放出能の上昇や、チオリン酸受容体を介した神経可塑性の変化を明らかにしています。
Figures are computed from collected data and may differ slightly.
Our findings indicate that the activity of DRN 5-HT neurons projecting to the VTA is a key modulator of balance between reward and aversion.
These results suggest the ketamine-induced serotonin release in medial prefrontal cortex is mediated by cholinergic neurons projecting from pedunculopontine tegmental nucleus to dorsal raphe nucleus via α4β2 nAChRs.
Major depressive disorder (MDD) is among the most common mental illnesses. Serotonergic (5-HT) neurons are central to the pathophysiology and treatment of MDD. Repeatedly recalling positive episodes is effective for MDD. Stimulating 5-HT neurons of the dorsal raphe nucleus (DRN) or neuronal ensembles in the dorsal dentate gyrus (dDG) associated with positive memories reverses the stress-induced behavioral abnormalities. Despite this phenotypic similarity, their causal relationship is unclear. Th
These results suggest that sustained exposure to SSRIs induces the augmentation of exocytotic 5-HT release, which is caused, at least in part, by the activation of AMPA/kainate receptors in the raphe slice cultures.
Most clinically-used antidepressants acutely increase monoamine levels in synaptic clefts, while their therapeutic effects often require several weeks of administration. Slow neuroadaptive changes in serotonergic neurons are considered to underlie this delayed onset of beneficial actions. Recently, we reported that sustained exposure of rat organotypic raphe slice cultures containing abundant serotonergic neurons to selective serotonin (5-HT) reuptake inhibitors (citalopram, fluoxetine and parox
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