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

•Ketamine increases freezing behavior in rats with experimental PTSD.•PTSD and ketamine treatment do not alter BDNF protein levels in rat brain.•PTSD and ketamine treatment do not alter glucose metabolism in rat brain. Acute treatment with ketamine, an NMDA receptor antagonist, has been reported to...

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Bibliographic Details
Published in:Neuroscience letters 2017-09, Vol.658, p.6-11
Main Authors: 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
Format: Article
Language:English
Subjects:
Amygdala
Animals
BDNF
Behavior, Animal - drug effects
Brain - metabolism
Brain-Derived Neurotrophic Factor - metabolism
Depressive Disorder - metabolism
Disease Models, Animal
Frontal cortex
Glucose - metabolism
Hippocampus
Ketamine - pharmacology
Male
microPET
PTSD
Rats, Wistar
Stress Disorders, Post-Traumatic - metabolism
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Summary:•Ketamine increases freezing behavior in rats with experimental PTSD.•PTSD and ketamine treatment do not alter BDNF protein levels in rat brain.•PTSD and ketamine treatment do not alter glucose metabolism in rat brain. 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.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2017.08.026