Ketamine promotes increased freezing behavior in rats with experimental PTSD without changing brain glucose metabolism or BDNF

NEUROSCIENCE LETTERS

卷:658

Article

Saur, Lisiani¹  Neves, Laura Tartari¹  Greggio, Samuel²  Venturin, Gianina Teribele²  Moriguchi Jeckel, Cristina Maria²  Da Costa, Jaderson Costa²  Bertoldi, Karine³  Schallenberger, Bruna³  Siqueira, Ionara Rodrigues³  Mestriner, Regis Gemerasca¹  Xavier, Leder Leal¹ 

[1] Pontificia Univ Catolica Rio Grande do Sul, FaBio, Lab Biol Celular & Tecidual, Porto Alegre, RS, Brazil

[2] Inst Cerebro Rio Grande do Sul PUCRS, Porto Alegre, RS, Brazil

[3] Univ Fed Rio Grande do Sul, ICBS, Dept Farmacol, Porto Alegre, RS, Brazil

关键词: PTSD;    Frontal cortex;    Hippocampus;    Amygdala;    microPET;    BDNF;   

DOI  :  10.1016/j.neulet.2017.08.026

来源: Elsevier

【 摘 要 】

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.

【 授权许可】

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