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Lin Sun

School of Psychology, Shandong Second Medical University, 7166# Baotong West Street, Weifang, Shandong 261053, PR China; Department of Neurosurgery, Shanting District People's Hospital, Beijing Road, New Town, Zaozhuang, Shandong 277200, PR China; Management Committee of Shanting Economic Development Zone, No.37, Fuqian Road, Zaozhuang, Shandong 277200, PR China. Electronic address: linsun2013@sdsmu.edu.cn.

4 papers in the library · 17 citations · publishing 2017-2025

Papers

Ketamine alleviates PTSD-like effect and improves hippocampal synaptic plasticity via regulation of GSK-3β/GR signaling of rats.

Journal of psychiatric research October 1, 2024 Zixun Wang, Xinyu Hu, Zhongyi Wang et al. 9 citations

Post-traumatic stress disorder affects 3-4% of people globally each year. In a rat model of PTSD induced by single prolonged stress, a single low dose of ketamine (10 mg/kg) prevented anxiety-like behaviors. Ketamine also reversed stress-induced changes in the hippocampus: it increased expression of glucocorticoid receptor, brain-derived neurotrophic factor, phosphorylated GSK-3β, FKBP5, and CRH, while decreasing GSK-3β protein expression, and it improved synaptic structure. A GSK-3β inhibitor produced similar behavioral effects, suggesting ketamine works by regulating GSK-3β/GR signaling to improve synaptic plasticity.

(2R, 6R)-hydroxynorketamine ameliorates PTSD-like behaviors during the reconsolidation phase of fear memory in rats by modulating the VGF/BDNF/GluA1 signaling pathway in the hippocampus.

Behavioural brain research January 5, 2025 Han Wang, Yuxuan He, Jiahao Tang et al. 5 citations

Injecting (2R,6R)-hydroxynorketamine ((2R,6R)-HNK) into the brain's lateral ventricle of rats with PTSD-like behaviors most effectively reduces anxiety and fear when given during the reconsolidation phase of fear memory—the period after a memory is recalled and before it is stored again. The drug restored levels of three proteins in the hippocampus (GluA1, VGF, and BDNF) that were lowered by stress and fear conditioning. No significant improvements occurred when the drug was given during the acquisition or extinction phases. The findings suggest that (2R,6R)-HNK works through the VGF/BDNF/GluA1 signaling pathway in the hippocampus to alleviate PTSD-like symptoms specifically during memory reconsolidation.

(2R,6R)-hydroxynorketamine alleviates PTSD-like endophenotypes by regulating the PI3K/AKT signaling pathway in rats.

Pharmacology, biochemistry, and behavior December 1, 2024 Lifen Liu, Rui Li, Lanxia Wu et al. 3 citations

In rats exposed to a combined stress model (single prolonged stress plus plantar shock), those treated with (2R,6R)-hydroxyketamine (HNK) showed reduced depression- and anxiety-like behaviors, including increased exploratory activity. The compound reversed stress-induced disruptions in the PI3K/AKT signaling pathway in the hippocampus and prefrontal cortex, but not in the amygdala. Traumatic stress itself altered PI3K/AKT signaling in all three brain regions. These results suggest that (2R,6R)-HNK may alleviate negative emotional symptoms after trauma by modulating PI3K/AKT signaling, particularly in the hippocampus.

Effects of short term low dose melatonin and ketamine on depressive behavior and BDNF expression in rats with chronic stress depression

Zhonghua xingwei yixue yu naokexue zazhi December 20, 2017 Haonan Li, Hongwei Sun, Yanyu Wang et al.

In a rat model of depression induced by chronic unpredictable mild stress, melatonin produced antidepressant-like effects comparable to those of ketamine. Rats exposed to 42 days of stress showed depressive-like behavior, indicated by reduced sucrose preference and increased immobility time in the forced swim test. After 14 days of treatment, both melatonin and ketamine significantly decreased immobility time and increased the number of BDNF-positive cells in the prefrontal cortex compared to stressed controls. Melatonin also increased BDNF cell counts more than ketamine did. However, only ketamine, not melatonin, significantly raised GluR1 cell counts. These findings suggest melatonin's antidepressant action may involve upregulation of BDNF.