Department of Psychiatry, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Institution of Neuroscience, Fourth Military Medical University, Xi'an 710032, China.
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Jul 13;93:171-181. doi: 10.1016/j.pnpbp.2019.03.018. Epub 2019 Apr 1.
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 (DAGLα) and cannabinoid type 1 receptor (CB1R) in the hippocampus with or without DAGLα 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 DAGLα 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, DAGLα and CB1R. However, either DAGLα 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 DAGLα 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 DAGLα and CB1R.
电针（EA）是一种临床有用的生理治疗方法，最近已被用于治疗多种脑部疾病。然而，早期 EA 干预在预防创伤后应激障碍（PTSD）中的潜在作用及其潜在的细胞和分子机制以前从未被研究过。在本研究中，我们使用增强型单次延长应激（ESPS）模型来评估早期 EA 干预对预防焦虑样和恐惧学习行为的影响，以及海马中突触后密度蛋白 95（PSD95）、突触小体蛋白（Syn）、脑源性神经营养因子（BDNF）、二酰基甘油脂肪酶α（DAGLα）和大麻素 1 型受体（CB1R）表达的影响，以及通过海马中的短发夹 RNA（shRNA）敲低 DAGLα 和 CB1R 对其表达的影响。此外，还观察了不同参数的电刺激对海马星形胶质细胞中 DAGLα 和 CB1R 表达的影响。结果表明，早期 EA 干预改善了海马突触可塑性，改善了 PTSD 样行为，并且还增加了 BDNF、DAGLα 和 CB1R 的表达。然而，通过短发夹 RNA（shRNA）敲低 DAGLα 或 CB1R 消除了早期 EA 干预的神经保护作用。此外，2/15Hz 1mA 的电刺激可提高 DAGLα 和 CB1R 的表达。总之，我们的研究结果提供了新的见解，表明早期 EA 干预有可能预防 PTSD，并且 EA 的保护作用涉及 DAGLα 和 CB1R 的激活。
