Deep brain stimulation of the amygdala alleviates post-traumatic stress disorder symptoms in a rat model

2010 ◽  
Vol 44 (16) ◽  
pp. 1241-1245 ◽  
Author(s):  
Jean-Philippe Langevin ◽  
Antonio A.F. De Salles ◽  
Hovsep P. Kosoyan ◽  
Scott E. Krahl
2022 ◽  
pp. 1-13
Author(s):  
Jennifer Meeres ◽  
Marwan Hariz

<b><i>Introduction:</i></b> Up to 30% of patients with post-traumatic stress disorder (PTSD), especially combat veterans, remain refractory to conventional treatment. For them, deep brain stimulation (DBS) has been suggested. Here, we review the literature on animal models of PTSD in which DBS has been used to treat PTSD-type behavior, and we review and discuss patient reports of DBS for PTSD. <b><i>Methods:</i></b> A broad search was performed to find experimental animal articles and clinical reports on PubMed, Ovid MEDLINE, Cochrane Library, and PsycINFO, using combinations and variations of search words pertinent to DBS and PTSD. <b><i>Results:</i></b> The search yielded 30 articles, 24 on DBS in rat models of PTSD, and 6 publications between 2016 and 2020 reporting on a total of 3 patients. DBS in rat models targeted 4 brain areas: medial prefrontal cortex (mPFC), ventral striatum, amygdala, and hippocampus. Clinical publications reported on 2 male combat veterans who received DBS in basolateral amygdala, and 1 female with PTSD due to domestic abuse, who received DBS of mPFC. All 3 patients benefitted to various extents from DBS, at follow-ups of 4 years, 6 months, and 7 months, respectively. <b><i>Conclusions:</i></b> PTSD is the only potential clinical indication for DBS that shows extensive animal research <i>prior</i> to human applications. Nevertheless, DBS for PTSD remains highly investigational. Despite several years of government funding of DBS research in view of treating severe PTSD in combat veterans, ethical dilemmas, recruitment difficulties, and issues related to use of DBS in such a complex and heterogenous disorder remain prevalent.


2015 ◽  
Vol 8 (2) ◽  
pp. 312 ◽  
Author(s):  
Ralph J. Koek ◽  
Jean-Philippe Langevin ◽  
Scottt E. Krahl ◽  
Holly N. Schwartz ◽  
James WY. Chen ◽  
...  

Synapse ◽  
2018 ◽  
Vol 72 (8) ◽  
pp. e22035 ◽  
Author(s):  
Onarae V. Rice ◽  
Charles R. Ashby ◽  
Clark Dixon ◽  
William Laurenzo ◽  
Jason Hayden ◽  
...  

Biomolecules ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 100 ◽  
Author(s):  
Laiali Alquraan ◽  
Karem H. Alzoubi ◽  
Hana Hammad ◽  
Suzie Y. Rababa’h ◽  
Fadia Mayyas

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that can happen after exposure to a traumatic event. Post-traumatic stress disorder is common among mental health disorders that include mood and anxiety disorders. Omega-3 fatty acids (OMGs) are essential for the maintenance of brain function and prevention of cognition dysfunctions. However, the possible effect of OMG on memory impairment induced by PTSD has not been studied. In here, such an effect was explored using a rat model of PTSD. The PTSD-like behavior was induced in animals using a single-prolonged stress (SPS) rat model of PTSD (2 h restraint, 20 min forced swimming, 15 min rest, 1–2 min diethyl ether exposure). The OMG was administered orally at a dose of 100 mg omega-3 polyunsaturated fatty acid (PUFA)/100 g body weight/day. Spatial learning and memory were assessed using the radial arm water maze (RAWM) method. Changes in oxidative stress biomarkers, thiobarbituric acid reactive substances (TBARS), and brain derived neuroptrophic factor (BDNF) in the hippocampus following treatments were measured. The results revealed that SPS impaired both short- and long-term memory (p < 0.05). Use of OMG prevented memory impairment induced by SPS. Furthermore, OMG normalized SPS induced changes in the hippocampus that reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratios, the activity of catalase, glutathione peroxidase (GPx), and TBARSs levels. In conclusion, the SPS model of PTSD-like behavior generated memory impairment, whereas OMG prevented this impairment, possibly through normalizing antioxidant mechanisms in the hippocampus.


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