Jun Yamada

Department of Anatomy and Neuroscience, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

2 papers in the library · 8 citations · publishing 2024-2025

Papers

Inhibition of reactive oxygen species production accompanying alternatively activated microglia by risperidone in a mouse ketamine model of schizophrenia.

Journal of neurochemistry September 1, 2024 Risako Fujikawa, Jun Yamada, Shoichiro Maeda et al. 6 citations

In a mouse model of schizophrenia, the antipsychotic risperidone reduced behavioral abnormalities and altered microglial activity and reactive oxygen species (ROS) in the hippocampus. Mice given ketamine showed schizophrenia-like behaviors, increased microglial density, and a shift toward more activated microglial shapes. Risperidone reversed these changes, lowering expression of the ROS-producing enzyme Nox2 and raising antioxidant enzyme levels. In isolated microglia, ketamine boosted ROS production, which risperidone blocked. A NOX2 inhibitor also counteracted ketamine-induced behavioral deficits, suggesting that reducing ROS via microglial modulation may help treat schizophrenia.

DOI: 10.1111/jnc.16133 Full text Ketamine Microglia Reactive oxygen species Risperidone +5

Tabernanthalog, a Non-Hallucinogenic Psychedelic, Alleviates Cancer-Induced Cognitive Deficits via Serotonergic Pathways

International Journal of Molecular Sciences August 4, 2025 Masahide Arinaga, Jun Yamada, Shoichiro Maeda et al. 2 citations

Cancer-related cognitive impairment (CRCI), which includes anxiety, depression, and memory deficits, reduces quality of life but is often underrecognized. In a mouse model of Lewis lung carcinoma, tabernanthalog (TBG), a non-hallucinogenic psychedelic analog, reversed anxiety-like behavior and memory impairment. Tumor-bearing mice had reduced tryptophan levels in blood and hippocampus, downregulated serotonergic receptor genes, and upregulated pro-inflammatory cytokine genes, along with increased microglial density and activation. TBG treatment normalized microglial density and morphology and restored serotonergic receptor and cytokine gene expression. In vitro, TBG partially suppressed neuroinflammatory gene expression in microglial cells exposed to tumor-conditioned medium. These findings suggest TBG alleviates CRCI-like symptoms by modulating neuroinflammation and microglial activation.

DOI: 10.3390/ijms26157519 Serotonergic Serotonin Neuroinflammation Hippocampal formation +5