Saur Lisiani, Neves Laura Tartari, Greggio Samuel, Venturin Gianina Teribele, Jeckel Cristina Maria Moriguchi, Costa Da Costa Jaderson, Bertoldi Karine, Schallenberger Bruna, Siqueira Ionara Rodrigues, Mestriner Régis Gemerasca, Xavier Léder Leal
Laboratório de Biologia Celular e Tecidual, FaBio, PUCRS, Porto Alegre, RS, Brazil.
Laboratório de Biologia Celular e Tecidual, FaBio, PUCRS, Porto Alegre, RS, Brazil.
Neurosci Lett. 2017 Sep 29;658:6-11. doi: 10.1016/j.neulet.2017.08.026. Epub 2017 Aug 18.
Acute treatment with ketamine, an NMDA receptor antagonist, has been reported to be efficacious in treating depression. The goal of our study was to evaluate ketamine treatment in an animal model of another important psychiatric disease, post-traumatic stress disorder (PTSD). Fifty-eight male rats were initially divided into four groups: Control+Saline (CTRL+SAL), Control+Ketamine (CTRL+KET), PTSD+Saline (PTSD+SAL) and PTSD+Ketamine (PTSD+KET). To mimic PTSD we employed the inescapable footshock protocol. The PTSD animals were classified according to freezing behavior duration into "extreme behavioral response" (EBR) or "minimal behavioral response" (MBR). Afterwards, the glucose metabolism and BDNF were evaluated in the hippocampus, frontal cortex, and amygdala. Our results show that animals classified as EBR exhibited increased freezing behavior and that ketamine treatment further increased freezing duration. Glucose metabolism and BDNF levels showed no significant differences. These results suggest ketamine might aggravate PTSD symptoms and that this effect is unrelated to alterations in glucose metabolism or BDNF protein levels.
据报道，N-甲基-D-天冬氨酸（NMDA）受体拮抗剂氯胺酮的急性治疗对抑郁症有效。我们研究的目的是在另一种重要的精神疾病——创伤后应激障碍（PTSD）的动物模型中评估氯胺酮治疗。58只雄性大鼠最初被分为四组：对照组+生理盐水（CTRL+SAL）、对照组+氯胺酮（CTRL+KET）、创伤后应激障碍组+生理盐水（PTSD+SAL）和创伤后应激障碍组+氯胺酮（PTSD+KET）。为模拟创伤后应激障碍，我们采用了不可逃避的足部电击方案。根据僵住行为持续时间，将创伤后应激障碍动物分为“极端行为反应”（EBR）或“最小行为反应”（MBR）。之后，在海马体、额叶皮质和杏仁核中评估葡萄糖代谢和脑源性神经营养因子（BDNF）。我们的结果表明，被归类为EBR的动物表现出增加的僵住行为，并且氯胺酮治疗进一步增加了僵住持续时间。葡萄糖代谢和BDNF水平没有显著差异。这些结果表明氯胺酮可能会加重创伤后应激障碍症状，并且这种作用与葡萄糖代谢或BDNF蛋白水平的改变无关。
