恐惧记忆难以抑制是创伤后应激障碍（PTSD）治疗的主要难点之一。全身麻醉药物应用于创伤患者是否影响恐惧记忆的巩固进而影响PTSD的发生是值得关注的问题。研究发现丙泊酚具有增强恐惧记忆的作用且与大麻素信号有关，但其作用脑区及神经环路机制仍不清楚。杏仁核在恐惧记忆形成和PTSD发病过程中发挥关键作用，证据表明丙泊酚可以增强麻醉状态下杏仁核的活动。杏仁核GABA能中间神经元高度表达大麻素受1型受体。我们推测丙泊酚可能通过增强大麻素信号抑制杏仁核局部GABA能神经元，使其对谷氨酸能神经元抑制减弱，从而增强杏仁核兴奋活动。本研究拟从整体行为-局部神经环路-细胞-分子多层次揭示丙泊酚可能通过大麻素介导杏仁核局部GABA环路去抑制，提高大鼠基底外侧杏仁核神经元兴奋性进而强化恐惧记忆巩固的神经机制。本项目的完成将为外科创伤人群合理选用麻醉药物提供理论依据，并为预防PTSD提供新的靶点和方向。

One of the main difficulty in the treatment of PTSD is hard to inhibit fear conditioning. It is worth asking whether general anesthetics have an impact on the consolidation of fear memory and thus influence PTSD. A researche showed that propofol enhanced the consolidation of fear memory by anandamide signal, but related brain regions and neural circuits are still unknown. The amygdala plays an important role in the formation of fear memory and pathological process of PTSD. The evidence indicated that propofol enhanced the activity of amygdala under anaesthesia. Cannabinoid receptor 1 (CB1) accumulated on GABAergic neurons in the amygdala. We hypothesize that propofol may inhibit GABAergic neurons by enhancing anandamide signal, which, in turn, result in weakening glutamatergic neurons inhibition. This research tries to elucidate the neural mechanism of propofol-enhanced fear memory in rats by the anandamide-induced disinhibition of GABA circuits in amygdala at the praxiology, local neural circuit, cell and biomolecule levels. The study will provide theoretical basis for clinical use of anaesthetics in trauma surgery patients and offer the new target and orientation for PTSD prevention.