@article{ref1,
title="Effects of oxytocin on fear memory and neuroinflammation in a rodent model of posttraumatic stress disorder",
journal="International journal of molecular sciences",
year="2018",
author="Wang, Sheng-Chiang and Lin, Chen-Cheng and Chen, Chun-Chuan and Tzeng, Nian-Sheng and Liu, Yia-Ping",
volume="19",
number="12",
pages="e19123848-e19123848",
abstract="Posttraumatic stress disorder (PTSD) is a trauma-induced mental disorder characterized by fear extinction abnormalities, which involve biological dysfunctions among fear circuit areas in the brain. Oxytocin (OXT) is a neuropeptide that regulates sexual reproduction and social interaction and has recently earned specific attention due to its role in adjusting neurobiological and behavioral correlates of PTSD; however, the mechanism by which this is achieved remains unclear. The present study aimed to examine whether the effects of OXT on traumatic stress-induced abnormalities of fear extinction (specifically induced by single prolonged stress (SPS), an animal model of PTSD) are associated with pro-inflammatory cytokines. Seven days after SPS, rats received intranasal OXT 40 min before a cue-dependent Pavlovian fear conditioning-extinction test in which rats' freezing degree was used to reflect the outcome of fear extinction. We also measured mRNA expression of <i>IL-1β</i>, <i>IFN-γ</i>, and <i>TNF-α</i> in the medial prefrontal cortex (mPFC), hippocampus, and amygdala at the end of the study, together with plasma oxytocin, corticosterone, IL-1β, IFN-γ, and TNF-α, to reflect the central and peripheral changes of stress-related hormones and cytokines after SPS. Our results suggested that intranasal OXT effectively amends the SPS-impaired behavior of fear extinction retrieval. Moreover, it neurochemically reverses the SPS increase in pro-inflammatory cytokines; thus, <i>IL-1β</i> and <i>IFN-γ</i> can be further blocked by the OXT antagonist atosiban (ASB) in the hippocampus. Peripheral profiles revealed a similar response pattern to SPS of OXT and corticosterone (CORT), and the SPS-induced increase in plasma levels of IL-1β and TNF-α could be reduced by OXT. The present study suggests potential therapeutic effects of OXT in both behavioral and neuroinflammatory profiles of PTSD.<p /> <p>Language: en</p>",
language="en",
issn="1661-6596",
doi="10.3390/ijms19123848",
url="http://dx.doi.org/10.3390/ijms19123848"
}