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Jiancheng Zhang

5 papers in the library · 72 citations · publishing 2019-2026

Papers

(R)-Ketamine Rapidly Ameliorates the Decreased Spine Density in the Medial Prefrontal Cortex and Hippocampus of Susceptible Mice After Chronic Social Defeat Stress

The International Journal of Neuropsychopharmacology August 28, 2019 Jiancheng Zhang, Youge Qu, Lijia Chang et al. 56 citations

A single injection of (R)-ketamine (10 mg/kg) rapidly reversed the loss of dendritic spines in the medial prefrontal cortex and hippocampus of mice that had become susceptible after chronic social defeat stress. Spine density was measured three hours after treatment and was significantly increased in the prelimbic area of the medial prefrontal cortex, the Cornu Ammonis3 region, and the dentate gyrus of the hippocampus. The findings suggest that (R)-ketamine's rapid restoration of spine density in these brain regions may underlie its fast-acting antidepressant effects.

Efficacy and safety of esketamine for emergency endotracheal intubation in ICU patients: a double-blind, randomized controlled clinical trial.

Scientific reports February 19, 2025 Xue Zhang, Xin Zhao, Jiaxin Xu et al. 8 citations

For emergency intubation in critically ill adults, using esketamine for induction results in higher mean arterial pressure during and after the procedure compared to a midazolam/sufentanil admixture, with no significant difference in heart rate. Patients receiving esketamine required less norepinephrine, had a shorter duration of ventilation support (median 105 vs. 212 hours), and a shorter ICU stay (median 7 vs. 15 days). 28-day mortality did not differ between groups, and no serious adverse events occurred. Esketamine appears to be a hemodynamically stable induction agent for this population.

Psychoactive substances for the treatment of neuropsychiatric disorders.

Asian journal of psychiatry November 1, 2024 Zifan Zhen, Xueqiang Sun, Shiying Yuan et al. 8 citations

A review of hallucinogens, MDMA, and ketamine for severe mental health disorders describes their mechanisms and clinical outcomes. Hallucinogens like LSD and psilocybin target 5-HT2A receptors, inducing perceptual shifts that aid therapy for depression and anxiety. MDMA influences serotonin, dopamine, and norepinephrine, alleviating PTSD symptoms by enhancing emotional engagement during psychotherapy. Ketamine, a glutamate receptor antagonist, rapidly relieves symptoms in treatment-resistant depression. These substances show promise for patients unresponsive to traditional treatments but require careful dosage, monitoring, and risk management to prevent abuse and adverse effects.

Pleiotropic modulation of the gut-brain-lung axis by ketamine and its enantiomers.

Molecular psychiatry April 13, 2026 Xin Zhao, Xinyu Zhang, Shiying Yuan et al.

Ketamine, a drug used for anesthesia and rapid antidepressant effects, also modulates systemic immunity and protects organs through interactions with the gut microbiota, microbial metabolites, and immune-cell trafficking. Along the gut-brain axis, ketamine restores microbial balance, normalizes short-chain fatty acid levels, and reduces migration of gut-derived immune cells to the central nervous system, correlating with reduced neuroinflammation and depressive-like behaviors. Through the gut-lung axis, ketamine limits bacterial translocation and reduces pulmonary infiltration of pro-inflammatory cells, suggesting potential relevance in acute lung injury. Arketamine appears to provide more sustained neuroprotection with fewer adverse effects than esketamine. The findings suggest broad therapeutic potential for neuropsychiatric and inflammatory diseases, but causal studies are needed.

Intestinal γδ T17-IL-17A signaling disrupts hippocampal mitophagy in stress-induced depression and is restored by arketamine.

Journal of neuroinflammation December 18, 2025 Mengqi Han, Bing Xie, Yuan Yu et al.

Chronic stress triggers depression by activating a gut-immune-brain pathway. In mice exposed to chronic restraint stress, gut microbiota changes caused small intestinal γδ T cells to migrate to the brain, where they released interleukin-17A (IL-17A). This IL-17A impaired a mitochondrial cleanup process called mitophagy in the hippocampus, leading to reduced energy production, damaged synapses, and depression-like behavior. Blocking γδ T cell migration, removing a key receptor on these cells, or giving the antidepressant arketamine all restored mitophagy and improved behavior. The findings identify a specific chain from gut microbes to immune cells to brain mitochondria that drives stress-induced depression, and point to arketamine as a potential treatment targeting this pathway.