氯胺酮
行为绝望测验
神经营养因子
开阔地
脑源性神经营养因子
高架加迷宫
前额叶皮质
焦虑
心理学
内科学
内分泌学
药理学
医学
神经科学
认知
精神科
受体
抗抑郁药
作者
Lanwei Hou,Yirui Qi,Hongwei Sun,Gang Wang,Qi Li,Yanyu Wang,Zuoji Zhang,Zhongde Du,Lin Sun
标识
DOI:10.1016/j.pnpbp.2018.03.019
摘要
Post-traumatic stress disorder (PTSD) is commonly associated with concurrent anxiety and depression symptoms, and reduce the expression of the Brain-Derived Neurotrophic Factor (BDNF) which promotes the proliferation and survival of neurons. The hyperpolarization-activated cyclic nucleotide-gated channel 1(HCN1) could be inhibited by the ketamine, a drug to alleviate depression and anxiety, and regulated the BDNF expression, however, the effects of ketamine in alleviating PTSD symptoms by regulating the HCN1-related BDNF have been poorly perceived. In the present study, the effects of ketamine were examined on the PTSD-like effects in a rat model of PTSD induced by SPS&S procedure. After the SPS&S procedure and model testing, PTSD rats were subjected to behavioral testing and biochemical assessments, followed by single treatment with certain doses of ketamine (5, 10, 15 and 20 mg/kg IP). The results showed that the SPS&S procedure induced severe PTSD-like behaviors, with lower levels of BDNF protein levels and higher level of the HCN1 protein in the prefrontal cortex (PFC). These were reversed by a single administration of ketamine. The ketamine with dose of 15 mg/kg significantly increased locomotor behavior in the open field test, aggrandized exploratory behavior in the elevated plus maze test, and decreased immobility time spent in the forced swim test. Meanwhile, ketamine with dose of 15 mg/kg could increase the BDNF protein level, while down-regulate the expression of the HCN1. Eventually, there was a negative correlation between the level of BDNF and HCN1 in the PFC. Ketamine affects the HCN1-related BDNF signaling pathways to alleviate PTSD-like effects in rat.
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