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Xiao-Hui Tang

2 papers in the library · 69 citations · publishing 2017-2022

Papers

Alterations in the inflammatory cytokines and brain-derived neurotrophic factor contribute to depression-like phenotype after spared nerve injury: improvement by ketamine

Scientific Reports June 5, 2017 Ze-Min Xie, Xingming Wang, Ning Xu et al. 69 citations

Rats with neuropathic pain that also developed depression-like behaviors had higher levels of pro-inflammatory cytokines (interleukin-1β and interleukin-6) and an imbalance between pro- and anti-inflammatory cytokines, along with lower levels of brain-derived neurotrophic factor in the prefrontal cortex, compared to rats without depression-like behaviors and sham-operated controls. A single dose of ketamine reversed both the depression-like behaviors and the elevated serum levels of IL-1β and IL-6. These findings suggest that changes in inflammatory cytokines and BDNF may underlie depression caused by neuropathic pain, and that serum cytokines could serve as biomarkers for ketamine's antidepressant effects.

A role of GABAA receptor α1 subunit in the hippocampus for rapid-acting antidepressant-like effects of ketamine.

Neuropharmacology December 21, 2022 Xiao-Hui Tang, Y. Diao, Zhuoying Ren et al.

Ketamine produces rapid antidepressant-like effects in mice exposed to forced swimming stress. The stressed mice showed depression-like behavior and reduced GABA levels in the hippocampus. Ketamine increased GABA and decreased glutamate there, and GABA levels correlated with behavior. Ketamine raised levels of certain GABAergic enzymes and transporters and astrocytic proteins, but not those on glutamatergic neurons. It also decreased the GABAAR α1 subunit, boosted GABA synthesis and metabolism, altered astrocyte plasticity, and increased ATP. A GABAAR antagonist or ATP itself had rapid antidepressant-like effects, while a GABAAR agonist blocked ketamine's effects. The findings suggest ketamine works by downregulating GABAAR α1, increasing GABA, and converting GABA to ATP.