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首页> 外文期刊>Progress in Neuro-Psychopharmacology & Biological Psychiatry: An International Research, Review and News Journal >Early intervention with electroacupuncture prevents PTSD-like behaviors in rats through enhancing hippocampal endocannabinoid signaling
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Early intervention with electroacupuncture prevents PTSD-like behaviors in rats through enhancing hippocampal endocannabinoid signaling

机译:利用电针提前干预通过增强海马内凸吲哚诺素信号传导来预防大鼠的PTSD样行为

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摘要

Electroacupuncture (EA) is a clinically useful physiological therapy that has been recently adopted to treat several brain disorders. However, the potential role of early EA intervention in the prevention of posttraumatic stress disorder (PTSD) as well as its potential cellular and molecular mechanism has never been investigated previously. In the present study, we used an enhanced single prolonged stress (ESPS) model to access the effects of early EA intervention on the prevention of anxiety-like and fear learning behaviors, as well as the influence of the expression of post-synaptic density protein 95 (PSD95), synaptophysin (Syn), brain derived neurotrophic factor (BDNF), diacylglycerol lipase alpha (DAGL alpha) and cannabinoid type 1 receptor (CB1R) in the hippocampus with or without DAGL alpha or CB1R knockdown by a short hairpin RNA (shRNA) in the hippocampus. Moreover, the effects of electrical stimulation with different parameters on the expression of DAGL alpha and CB1R in the hippocampal astrocytes were also observed. The results showed that Early EA intervention improved hippocampal synaptic plasticity and ameliorated PTSD-like behaviors and also increased expression of BDNF, DAGL alpha and CB1R. However, either DAGL alpha or CB1R knockdown by a short hairpin RNA (shRNA) eliminated the neuroprotective effects of early EA intervention. Furthermore, electrical stimulation with 2/15 Hz 1 mA elevated the expression of DAGL alpha and CB1R. Altogether, our findings provide new insights regarding the possibility of using early EA intervention in the prevention of PTSD, and the protective effects of EA is involving the activation of DAGL alpha and CB1R.
机译:电针(EA)是最近采用的临床有用的生理治疗治疗几种脑疾病。然而,早期EA干预在预防失基应激障碍(PTSD)中的潜在作用以及以前从未研究过其潜在的细胞和分子机制。在本研究中,我们使用了增强的单一长期压力(ESP)模型来获得早期EA干预对预防焦虑和恐惧学习行为的影响,以及突触后密度蛋白表达的影响95(PSD95),突触蛋白(SYN),脑衍生的神经营养因子(BDNF),二酰基甘油脂肪酶α(DAGLα)和大麻素型1型受体(CB1R)在海马中,有或没有DAGLα或CB1R通过短发夹RNA敲低( shrna)在海马中。此外,还观察到对不同参数对海马星形细胞中DAGLα和CB1R表达的不同参数的影响。结果表明,早期EA干预改善了海马突触可塑性和改善的可接触的PTSD样行为,也增加了BDNF,DAGLα和CB1R的表达。然而,DAGLα或CB1R通过短发夹RNA(ShRNA)敲低,消除了早期EA干预的神经保护作用。此外,用2/15Hz 1 mA的电刺激升高了DAGLα和CB1R的表达。完全,我们的研究结果提供了有关使用早期EA干预的可能性在预防PTSD中的可能性,并且EA的保护作用涉及激活DAGLα和CB1R。

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