@article{Saur2017,
abstract = {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.},
author = {Saur, Lisiani and Neves, Laura Tartari and Greggio, Samuel and Venturin, Gianina Teribele and Jeckel, Cristina Maria Moriguchi and {Costa Da Costa}, Jaderson and Bertoldi, Karine and Schallenberger, Bruna and Siqueira, Ionara Rodrigues and Mestriner, R{\'{e}}gis Gemerasca and Xavier, L{\'{e}}der Leal},
doi = {10.1016/j.neulet.2017.08.026},
journal = {Neurosci. Lett.},
keywords = {CA},
mendeley-tags = {CA},
month = {sep},
pages = {6--11},
title = {{Ketamine promotes increased freezing behavior in rats with experimental PTSD without changing brain glucose metabolism or BDNF}},
url = {http://linkinghub.elsevier.com/retrieve/pii/S0304394017306742},
volume = {658},
year = {2017}
}

{"_id":"Wh2zbLMj9XXa87Hdv","bibbaseid":"saur-neves-greggio-venturin-jeckel-costadacosta-bertoldi-schallenberger-etal-ketaminepromotesincreasedfreezingbehaviorinratswithexperimentalptsdwithoutchangingbrainglucosemetabolismorbdnf-2017","downloads":0,"creationDate":"2017-08-29T20:29:02.688Z","title":"Ketamine promotes increased freezing behavior in rats with experimental PTSD without changing brain glucose metabolism or BDNF","author_short":["Saur, L.","Neves, L. T.","Greggio, S.","Venturin, G. T.","Jeckel, C. M. M.","Costa Da Costa, J.","Bertoldi, K.","Schallenberger, B.","Siqueira, I. R.","Mestriner, R. G.","Xavier, L. L."],"year":2017,"bibtype":"article","biburl":"https://mind-foundation.org/wp-content/uploads/2017/09/04.09.2017 ASC-Study-Monitor.bib","bibdata":{"bibtype":"article","type":"article","abstract":"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.","author":[{"propositions":[],"lastnames":["Saur"],"firstnames":["Lisiani"],"suffixes":[]},{"propositions":[],"lastnames":["Neves"],"firstnames":["Laura","Tartari"],"suffixes":[]},{"propositions":[],"lastnames":["Greggio"],"firstnames":["Samuel"],"suffixes":[]},{"propositions":[],"lastnames":["Venturin"],"firstnames":["Gianina","Teribele"],"suffixes":[]},{"propositions":[],"lastnames":["Jeckel"],"firstnames":["Cristina","Maria","Moriguchi"],"suffixes":[]},{"propositions":[],"lastnames":["Costa Da Costa"],"firstnames":["Jaderson"],"suffixes":[]},{"propositions":[],"lastnames":["Bertoldi"],"firstnames":["Karine"],"suffixes":[]},{"propositions":[],"lastnames":["Schallenberger"],"firstnames":["Bruna"],"suffixes":[]},{"propositions":[],"lastnames":["Siqueira"],"firstnames":["Ionara","Rodrigues"],"suffixes":[]},{"propositions":[],"lastnames":["Mestriner"],"firstnames":["Régis","Gemerasca"],"suffixes":[]},{"propositions":[],"lastnames":["Xavier"],"firstnames":["Léder","Leal"],"suffixes":[]}],"doi":"10.1016/j.neulet.2017.08.026","journal":"Neurosci. Lett.","keywords":"CA","mendeley-tags":"CA","month":"sep","pages":"6–11","title":"Ketamine promotes increased freezing behavior in rats with experimental PTSD without changing brain glucose metabolism or BDNF","url":"http://linkinghub.elsevier.com/retrieve/pii/S0304394017306742","volume":"658","year":"2017","bibtex":"@article{Saur2017,\nabstract = {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.},\nauthor = {Saur, Lisiani and Neves, Laura Tartari and Greggio, Samuel and Venturin, Gianina Teribele and Jeckel, Cristina Maria Moriguchi and {Costa Da Costa}, Jaderson and Bertoldi, Karine and Schallenberger, Bruna and Siqueira, Ionara Rodrigues and Mestriner, R{\\'{e}}gis Gemerasca and Xavier, L{\\'{e}}der Leal},\ndoi = {10.1016/j.neulet.2017.08.026},\njournal = {Neurosci. Lett.},\nkeywords = {CA},\nmendeley-tags = {CA},\nmonth = {sep},\npages = {6--11},\ntitle = {{Ketamine promotes increased freezing behavior in rats with experimental PTSD without changing brain glucose metabolism or BDNF}},\nurl = {http://linkinghub.elsevier.com/retrieve/pii/S0304394017306742},\nvolume = {658},\nyear = {2017}\n}\n","author_short":["Saur, L.","Neves, L. T.","Greggio, S.","Venturin, G. T.","Jeckel, C. M. M.","Costa Da Costa, J.","Bertoldi, K.","Schallenberger, B.","Siqueira, I. R.","Mestriner, R. G.","Xavier, L. L."],"key":"Saur2017","id":"Saur2017","bibbaseid":"saur-neves-greggio-venturin-jeckel-costadacosta-bertoldi-schallenberger-etal-ketaminepromotesincreasedfreezingbehaviorinratswithexperimentalptsdwithoutchangingbrainglucosemetabolismorbdnf-2017","role":"author","urls":{"Paper":"http://linkinghub.elsevier.com/retrieve/pii/S0304394017306742"},"keyword":["CA"],"downloads":0},"search_terms":["ketamine","promotes","increased","freezing","behavior","rats","experimental","ptsd","without","changing","brain","glucose","metabolism","bdnf","saur","neves","greggio","venturin","jeckel","costa da costa","bertoldi","schallenberger","siqueira","mestriner","xavier"],"keywords":["ca","amygdala","bdnf","frontal cortex","hippocampus","ptsd","micropet"],"authorIDs":[],"dataSources":["nZgrskreN65H4K49p"]}