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Journal articles on the topic 'PTSD animal model'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Ivanišević, Milica, Milica Knežević, Natalija Kojović, and Ana Starčević. "Volumetric analysis of hippocampus and amygdala in animal model of PTSD." Medicinski podmladak 73, no. 1 (2022): 25–29. http://dx.doi.org/10.5937/mp73-33408.

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Introduction: Posttraumatic stress disorder (PTSD) represents a mental disorder that occurs after life threatening situations. Animal models in psychiatry studies represent a base from which results and conclusions can be translated to human population. Amygdala and hippocampus are important neuroanatomical substrates possibly relevant to PTSD pathogenesis. Aim: The aim of study was to investigate volumetric changes that occur in hippocampus and amygdala related to PTSD animal model. Material and methods: Experiment was conducted on adult male Wistar rats. They were two groups, experimental and control. Experimental paradigm lasted for 31 days during which animals were exposed to acute and chronic stress. Acute stress was performed on the first day and ten days later. In between, animals were exposed to chronic social stress by pair rotations. Before second acute stress exposure, experimental group was divided in two subgroups from which one received dexamethasone dose. After the experiment ended, animals were sacrificed and the brain was extracted. Following the freezing process, brain tissue samples were cut and prepared for microscopy using. This was followed by volumetric analysis of hippocampus and amygdala. Measurements were performed bilaterally using Image Tool 3.0 Software. Results: Results showed volumetric changes in these structures. Hippocampus had smaller volume in the experimental subgroup without dexamethasone (x̄ = 0.6144) compared to the control group (x̄ = 0.9688). Amygdala, as well, had smaller volumes in same subgroup compared to the control (x̄ = 10.0156 compared to x̄ = 11.5041). Conclusion: Our study provided results in agreement with several previous studies on rodents and contributes to the assumption that hippocampus and amygdala have significance in PTSD etiology. Further goal is to expand our study which will help us to better understand the disorder itself.

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Perez-Garcia, Georgina, Miguel A. Gama Sosa, Rita De Gasperi, Anna E. Tschiffely, Richard M. McCarron, Patrick R. Hof, Sam Gandy, Stephen T. Ahlers, and Gregory A. Elder. "Blast-induced "PTSD": Evidence from an animal model." Neuropharmacology 145 (February 2019): 220–29. http://dx.doi.org/10.1016/j.neuropharm.2018.09.023.

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Zhan, Bo, Yingxin Zhu, Jianxun Xia, Wenfu Li, Ying Tang, Anju Beesetty, Jiang-Hong Ye, and Rao Fu. "Comorbidity of Post-Traumatic Stress Disorder and Alcohol Use Disorder: Animal Models and Associated Neurocircuitry." International Journal of Molecular Sciences 24, no. 1 (December 26, 2022): 388. http://dx.doi.org/10.3390/ijms24010388.

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Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are prevalent neuropsychiatric disorders and frequently co-occur concomitantly. Individuals suffering from this dual diagnosis often exhibit increased symptom severity and poorer treatment outcomes than those with only one of these diseases. Lacking standard preclinical models limited the exploration of neurobiological mechanisms underlying PTSD and AUD comorbidity. In this review, we summarize well-accepted preclinical model paradigms and criteria for developing successful models of comorbidity. We also outline how PTSD and AUD affect each other bidirectionally in the nervous nuclei have been heatedly discussed recently. We hope to provide potential recommendations for future research.

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Cohen, Hagit, and Rachel Yehuda. "Gender Differences in Animal Models of Posttraumatic Stress Disorder." Disease Markers 30, no. 2-3 (2011): 141–50. http://dx.doi.org/10.1155/2011/734372.

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Epidemiological studies report higher prevalence rates of stress-related disorders such as acute stress disorder and post-traumatic stress disorder (PTSD) in women than in men following exposure to trauma. It is still not clear whether this greater prevalence in woman reflects a greater vulnerability to stress-related psychopathology. A number of individual and trauma-related characteristics have been hypothesized to contribute to these gender differences in physiological and psychological responses to trauma, differences in appraisal, interpretation or experience of threat, coping style or social support. In this context, the use of an animal model for PTSD to analyze some of these gender-related differences may be of particular utility. Animal models of PTSD offer the opportunity to distinguish between biological and socio-cultural factors, which so often enter the discussion about gender differences in PTSD prevalence.In this review, we present and discuss sex-differences in behavioral, neurochemical, neurobiological and pharmacological findings that we have collected from several different animal studies related to both basal conditions and stress responses. These models have used different paradigms and have elicited a range of behavioral and physiological manifestations associated with gender. The overall data presented demonstrate that male animals are significantly more vulnerable to acute and chronic stress, whereas females are far more resilient. The stark contradiction between these findings and contemporary epidemiological data regarding human subjects is worthy of further study. The examination of these gender-related differences can deepen our understanding of the risk or the pathophysiology of stress-related disorders.

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Cohen, Hagit, Nitsan Kozlovsky, Cramer Alona, Michael A. Matar, and Zohar Joseph. "Animal model for PTSD: From clinical concept to translational research." Neuropharmacology 62, no. 2 (February 2012): 715–24. http://dx.doi.org/10.1016/j.neuropharm.2011.04.023.

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6

Liberzon, I., M. Krstov, and E. A. Young. "Stress — Restress: An animal model of HPA abnormalities in PTSD." Biological Psychiatry 39, no. 7 (April 1996): 567. http://dx.doi.org/10.1016/0006-3223(96)84177-1.

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7

Starcevic, Ana, Sasa Petricevic, Vuk Djulejic, Zoran Radojicic, Branislav Starcevic, and Branislav Filipovic. "Effects of Chronic Psychosocial Stress on Reduction of Basal Glucocorticoid Levels and Suppression of Glucocorticoid Levels Following Dexamethasone Administration in Animal Model of PTSD." Open Access Macedonian Journal of Medical Sciences 2, no. 1 (March 15, 2014): 18–22. http://dx.doi.org/10.3889/oamjms.2014.003.

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Aim: To further examine the neurobiological mechanisms and their outcomes responsible for the PTSD sequelae induced by laboratory animal model and to explore the effects of chronic psychosocial paradigm. We tested the hypothesis that our animal model of PTSD would display abnormalities in glucocorticoid levels that are manifest in people with PTSD and that psychosocially stressed rats exhibit a significantly greater suppression of corticosterone levels than control rats following the administration of dexamethasone.Methods: Animals were divided into two groups. The experimental group was scheduled to exposure to two types of stressors: double exposure to acute immobilization stress, and combined predator-threat stress and daily social stress. There was also administration of dexamethasone in combination with stress exposure.Results: There was a statistical difference between masses of thymus in the stress group and stress group with dexamethasone appliance (p=0.024). We found statistical significance between baseline cortisol and stress induced levels of cortisol and between stress induced group and return to baseline group.Conclusion: Significant changes in HPA activity, reductions in basal glucocorticoid levels and enhanced dexamethasone induced inhibition of glucocorticoid levels have been manifested. All of this is manifested in PTSD patients also as many other stress induces changes.

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Brand, Sarel Jacobus, and Brian Herbert Harvey. "Exploring a post-traumatic stress disorder paradigm in Flinders sensitive line rats to model treatment-resistant depression I: bio-behavioural validation and response to imipramine." Acta Neuropsychiatrica 29, no. 4 (August 30, 2016): 193–206. http://dx.doi.org/10.1017/neu.2016.44.

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ObjectiveCo-morbid depression with post-traumatic stress disorder (PTSD) is often treatment resistant. In developing a preclinical model of treatment-resistant depression (TRD), we combined animal models of depression and PTSD to produce an animal with more severe as well as treatment-resistant depressive-like behaviours.MethodsMale Flinders sensitive line (FSL) rats, a genetic animal model of depression, were exposed to a stress re-stress model of PTSD [time-dependent sensitisation (TDS)] and compared with stress-naive controls. Seven days after TDS stress, depressive-like and coping behaviours as well as hippocampal and cortical noradrenaline (NA) and 5-hydroxyindoleacetic acid (5HIAA) levels were analysed. Response to sub-chronic imipramine treatment (IMI; 10 mg/kg s.c.×7 days) was subsequently studied.ResultsFSL rats demonstrated bio-behavioural characteristics of depression. Exposure to TDS stress in FSL rats correlated negatively with weight gain, while demonstrating reduced swimming behaviour and increased immobility versus unstressed FSL rats. IMI significantly reversed depressive-like (immobility) behaviour and enhanced active coping behaviour (swimming and climbing) in FSL rats. The latter was significantly attenuated in FSL rats exposed to TDS versus unstressed FSL rats. IMI reversed reduced 5HIAA levels in unstressed FSL rats, whereas exposure to TDS negated this effect. Lowered NA levels in FSL rats were sustained after TDS with IMI significantly reversing this in the hippocampus.ConclusionCombining a gene-X-environment model of depression with a PTSD paradigm produces exaggerated depressive-like symptoms that display an attenuated response to antidepressant treatment. This work confirms combining FSL rats with TDS exposure as a putative animal model of TRD.

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Jia, Min, Stanley E. Smerin, Lei Zhang, Guoqiang Xing, Xiaoxia Li, David Benedek, Robert Ursano, and He Li. "Corticosterone mitigates the stress response in an animal model of PTSD." Journal of Psychiatric Research 60 (January 2015): 29–39. http://dx.doi.org/10.1016/j.jpsychires.2014.09.020.

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Hashimoto, Takashi, Ken-ichi Matsuda, and Mitsuhiro Kawata. "Expression analyses of CRH in the brain of PTSD animal model." Neuroscience Research 71 (September 2011): e368. http://dx.doi.org/10.1016/j.neures.2011.07.1615.

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Xu, Jia-ning, Li-fang Chen, Jun Su, Zhi-li Liu, Jie Chen, Qing-fen Lin, Wei-dong Mao, Zhuo-wei Gao, and Dong Shen. "The anxiolytic-like effects of estazolam on a PTSD animal model." Psychiatry Research 269 (November 2018): 529–35. http://dx.doi.org/10.1016/j.psychres.2018.08.118.

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Khan, Samir, and Israel Liberzon. "Topiramate attenuates exaggerated acoustic startle in an animal model of PTSD." Psychopharmacology 172, no. 2 (March 1, 2004): 225–29. http://dx.doi.org/10.1007/s00213-003-1634-4.

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Yabuki, Yasushi, and Kohji Fukunaga. "Clinical Therapeutic Strategy and Neuronal Mechanism Underlying Post-Traumatic Stress Disorder (PTSD)." International Journal of Molecular Sciences 20, no. 15 (July 24, 2019): 3614. http://dx.doi.org/10.3390/ijms20153614.

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Post-traumatic stress disorder (PTSD) is characterized by an exaggerated response to contextual memory and impaired fear extinction, with or without mild cognitive impairment, learning deficits, and nightmares. PTSD is often developed by traumatic events, such as war, terrorist attack, natural calamities, etc. Clinical and animal studies suggest that aberrant susceptibility of emotion- and fear-related neurocircuits, including the amygdala, prefrontal cortex (PFC), and hippocampus may contribute to the development and retention of PTSD symptoms. Psychological and pharmacological therapy, such as cognitive behavioral therapy (CBT), and treatment with anti-depressive agents and/or antipsychotics significantly attenuate PTSD symptoms. However, more effective therapeutics are required for improvement of quality of life in PTSD patients. Previous studies have reported that ω3 long-chain polyunsaturated fatty acid (LCPUFA) supplements can suppress the development of PTSD symptoms. Fatty acid binding proteins (FABPs) are essential for LCPUFA intracellular trafficking. In this review, we have introduced Fabp3 null mice as an animal model of PTSD with impaired fear extinction. Moreover, we have addressed the neuronal circuits and novel therapeutic strategies for PTSD symptoms.

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Nova Mahendra, Agung, and I. Nyoman Adi Jaya Putra. "Hippocampal Endoplasmic Reticulum Stress: Novel Target in PTSD Pharmacotherapy?" Biomedical and Pharmacology Journal 11, no. 3 (September 6, 2018): 1269–74. http://dx.doi.org/10.13005/bpj/1488.

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Posttraumatic stress disorder (PTSD) is an anxiety disorder that occurred in individual who had experienced severe traumatic stresses. This disorder is accompanied by functional impairments in daily activities, comorbidities (such as depression) and increased risk of suicide. Some studies also demonstrate that PTSD is linked to structural and functional impairment of hippocampus. Hippocampal defect has been found in PTSD model, especially in single-prolonged stress (SPS)-induced animal model, with excessive or prolonged endoplasmic reticulum (ER) stress-induced neuronal apoptosis as a proposed mechanism. Unfortunately, this cellular event has not been studied and validated in humans suffering from PTSD. Two chaperones known as glucose-regulated protein 78 (GRP78) and sigma-1 receptor (Sig1R) have been demonstrated to exhibit central roles in mitigating the effects of severe ER stress on cell survival. Several selective serotonin-reuptake inhibitors (SSRIs), such as fluvoxamine and sertraline, are also found to be an agonist and antagonist of sigma-1 receptor (Sig1R) in animal brain cells, respectively. There is also link between antidepressant use and risk of suicidal ideation. Therefore, the authors propose that hippocampal ER stress may be involved in PTSD pathobiology. Pharmacodynamics of currently available therapeutic agents for PTSD and its comorbidities on hippocampal ER stress should be clearly elucidated to promote therapy optimization and drug development.

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Mackie, P. M., C. Wilkinson, A. Gopinath, L. Knackstedt, and H. Khoshbouei. "30580 A TL1 Approach to Assessing Peripheral Immune Changes in PTSD." Journal of Clinical and Translational Science 5, s1 (March 2021): 88. http://dx.doi.org/10.1017/cts.2021.628.

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ABSTRACT IMPACT: We present preliminary data and an outlined approach to assess peripheral immune changes associated with PTSD in a clinical setting and in a pre-clinical rat model of PTSD. OBJECTIVES/GOALS: We report our methodology and findings indicating a relationship between CNS dopamine signaling and peripheral immune cell populations and propose to extend this methodology to a PTSD patient population to elucidate immune-brain connections in this disorder. METHODS/STUDY POPULATION: Using an IRB-approved protocol in collaboration with a board-certified psychiatrist, we will recruit PTSD patients undergoing treatment, newly diagnosed drug-naiive PTSD patients, and age-matched healthy controls. Flow cytometry will be used for immunophenotyping on blood samples from each group. To complement this data, we will also measure serum cytokine levels in each group. In order to elucidate the connection between the observed immunophenotypes in the PTSD population and CNS neurotransmitters levels, we will employ a rodent model of PTSD and high-pressure liquid chromatography to measure dopamine levels in tandem with peripheral immune changes. RESULTS/ANTICIPATED RESULTS: In both humans and rodents with low CNS dopamine, an expansion of monocyte-derived suppressor cells was observed via flow cytometry. We anticipate that human PTSD patients will exhibit a similar expansion in suppressive immune cells’‘ in agreement with existing literature suggesting a chronic inflammatory state in PTSD. Moreover, in an animal model of PTSD we anticipate an inverse correlation between the CNS dopamine levels and the size of the immune suppressor cell population. DISCUSSION/SIGNIFICANCE OF FINDINGS: Our findings will indicate whether altered dopamine neurotransmission underlies peripheral immune system changes in the context of PTSD models and human patients. Thus, these findings will provide an alternative avenue for future investigations on the role of the immune system in PTSD.

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Su, Ai-shan, Jun-wei Zhang, and Jing Zou. "The anxiolytic-like effects of puerarin on an animal model of PTSD." Biomedicine & Pharmacotherapy 115 (July 2019): 108978. http://dx.doi.org/10.1016/j.biopha.2019.108978.

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Connor, Kathryn M., and Jonathan R. T. Davidson. "The Role of Serotonin in Posttraumatic Stress Disorder: Neurobiology and Pharmacotherapy." CNS Spectrums 3, S2 (August 1998): 42–51. http://dx.doi.org/10.1017/s1092852900007318.

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AbstractMuch attention has been given to the role of catecholamine dysfunction in posttraumatic stress disorder (PTSD), and only recently have researchers begun to focus on serotonin (5-HT) in PTSD. Serotonin appears to be a factor in responses followin extreme stress, such as those that precede PTSD. In this review, the authors provide a brief overview of the concept of PTSD and specific issues of clinical concern. The role 5-HT in the neurobiology of PTSD is explored in a review of animal model studies and of clinical investigations of paroxetine binding, pharmacologic challenges, and neuroimaging. Data on the use of 5-HT in PTSD treatment are provided in a review of both open-label and controlled studies of serotonergically active drugs.

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18

Lee, Dong-Hun, Ji-Young Lee, Dong-Yong Hong, Eun-Chae Lee, Sang-Won Park, Man-Ryul Lee, and Jae-Sang Oh. "Neuroinflammation in Post-Traumatic Stress Disorder." Biomedicines 10, no. 5 (April 20, 2022): 953. http://dx.doi.org/10.3390/biomedicines10050953.

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Post-traumatic stress disorder (PTSD) is a well-known mental illness, which is caused by various stressors, including memories of past physical assaults and psychological pressure. It is diagnosed as a mental and behavioral disorder, but increasing evidence is linking it to the immune system and inflammatory response. Studies on the relationship between inflammation and PTSD revealed that patients with PTSD had increased levels of inflammatory cytokine biomarkers, such as interleukin-1, interleukin-6, tumor necrosis factor-α, nuclear factor-κB, and C-reactive protein, compared with healthy controls. In addition, animal model experiments imitating PTSD patients suggested the role of inflammation in the pathogenesis and pathophysiology of PTSD. In this review, we summarize the definition of PTSD and its association with increased inflammation, its mechanisms, and future predictable diseases and treatment possibilities. We also discuss anti-inflammatory treatments to address inflammation in PTSD.

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COHEN, H. "The Contribution of an Animal Model Toward Uncovering Biological Risk Factors for PTSD." Annals of the New York Academy of Sciences 1071, no. 1 (July 1, 2006): 335–50. http://dx.doi.org/10.1196/annals.1364.026.

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Gao, Zhuo-wei, Rong-Le Ju, Min Luo, Shu-lian Wu, and Wen-Tong Zhang. "The anxiolytic-like effects of ginsenoside Rg2 on an animal model of PTSD." Psychiatry Research 279 (September 2019): 130–37. http://dx.doi.org/10.1016/j.psychres.2018.12.034.

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Dengler, Bradley A., Shane A. Hawksworth, Laura Berardo, Ian McDougall, and Alexander M. Papanastassiou. "Bilateral amygdala stimulation reduces avoidance behavior in a predator scent posttraumatic stress disorder model." Neurosurgical Focus 45, no. 2 (August 2018): E16. http://dx.doi.org/10.3171/2018.5.focus18166.

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OBJECTIVEThe predator scent model of posttraumatic stress disorder (PTSD) produces prolonged abnormal anxiety and avoidance-like behaviors. Increased basolateral amygdala activity has been shown to correlate with severity of PTSD symptoms in human studies. Modulation of this increased amygdala activity by deep brain stimulation led to improved symptoms in prior studies that used a foot shock model of inducing PTSD. The predator scent model is a different technique that induces long-lasting avoidance behavioral responses by exposing the animal to an inescapable scent of one of its predators. The authors hypothesize that high-frequency stimulation of the bilateral basolateral amygdala will decrease avoidance and anxiety-like behaviors in a predator scent rodent model of PTSD.METHODSRodents underwent cat urine exposure in a place preference protocol. Avoidance in the place preference paradigm and anxiety-like behavior in the elevated plus maze were measured before and after high-frequency stimulation.RESULTSPredator scent exposure resulted in long-term significant avoidance behavior in rodents. Bilateral stimulation significantly decreased avoidance behavior in rodents compared to no stimulation following predator scent exposure. There were no significant differences in anxiety behaviors on the elevated plus maze between stimulated and unstimulated cohorts.CONCLUSIONSBilateral stimulation of the basolateral amygdala leads to decreased avoidance behavior compared to controls in a predator scent model of PTSD.

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Bleiberg, James, Maurice Prout, Dennis Debiak, Carin Lefkowitz, and Indira Paharia. "Animal-Assisted Prolonged Exposure: A Treatment for Survivors of Sexual Assault Suffering Posttraumatic Stress Disorder." Society & Animals 13, no. 4 (2005): 275–96. http://dx.doi.org/10.1163/156853005774653654.

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AbstractThis paper proposes the development of a new model of treatment for survivors of sexual abuse suffering from Posttraumatic Stress Disorder (PTSD). Foa, Rothbaum, Riggs, and Murdock (1991) and Foa, Rothbaum, and Furr (2003) support Prolonged Exposure (PE) as a highly effective treatment for PTSD. However, PE can be intimidating to survivors, contributing to hesitancy to participate in the treatment. This paper posits that animal-assisted therapy (AAT) will decrease anxiety, lower physiological arousal, enhance the therapeutic alliance, and promote social lubrication. The paper also posits that AAT will enhance the value of PE by making it more accessible to survivors, increasing social interaction, and perhaps decreasing the number of sessions required for habituation to the traumatic memories.

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Bali, Anjana, and Amteshwar Singh Jaggi. "Electric foot shock stress: a useful tool in neuropsychiatric studies." Reviews in the Neurosciences 26, no. 6 (December 1, 2015): 655–77. http://dx.doi.org/10.1515/revneuro-2015-0015.

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AbstractElectric foot shock is a complex stressor with both physical and emotional components. It has been employed as an important tool to develop diverse animal models in the field of psychopharmacology. The electric foot shock paradigm includes acute or chronic exposures of shocks of varying intensity and duration on an electrified grid floor in an electric foot shock apparatus. Research evidence reveals that foot shocks of varying intensity produce behavioral and neurochemical changes reflecting depression, anxiety, and post-traumatic stress disorder (PTSD) in humans. Animals generally do not habituate to foot shocks in comparison to other stressors, including loud noise, bright light, and hot and cold temperatures. Additionally, it offers an experimental advantage of control over intensity and duration; therefore, by varying its application parameters, different disorder models have been created. Electric foot shock fear conditioning-induced ultrasonic vocalization and fear-potentiated startle have been explored to develop models of anxiety and panic. Similarly, fear conditioning in the form of foot shock exposure followed by situational reminders has been used to develop a model of PTSD. Electric foot shock-induced conflict has been explored to develop operant conflict models (Geller-Seifter and Vogel tests), which in turn are pharmacologically validated to screen potential anti-anxiety agents. Inescapable electric shock-induced ‘learned helplessness’ mimics the symptomology of depression, and this phenomenon has been employed to develop the model of depression. The present review describes the pharmacologically validated models of anxiety, depression, and PTSD involving electric foot shock as an aversive stimulus.

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Li, M. X., F. Han, J. D. Liu, and X. Y. Shi. "Single-prolonged stress induced mitochondrial - dependent apoptosis in hippocampus in the rat model of post-traumatic stress disorder." European Psychiatry 26, S2 (March 2011): 1083. http://dx.doi.org/10.1016/s0924-9338(11)72788-2.

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ObjectiveThe aim of this study was to reveal the possible mechanisms involved in apoptosis induced by single prolonged stress (SPS) in hippocampus of post-traumatic stress disorder (PTSD) rats.MethodsSPS is one of the animal models proposed for PTSD. Wistar rats were killed at 1, 4, 7, 14 and 28days after exposure to SPS. Expression of caspase-9, caspase-3, cytochrome c, Bcl-2 and Bax was detected by immunohistochemistry, immunofluorescence, western blotting and electron microscopy. Apoptotic cells were assessed by TUNEL method.ResultsOur results showed apoptotic cells were significantly increased in hippocampus of SPS rats, accompanied by release of cytochrome c from the mitochondria into the cytosol, increase of caspase-9 and caspase-3 expression and decrease of the Bcl-2 / Bax ratio.ConclusionThe results indicate that SPS induced apoptosis in hippocampus of PTSD rats, and the mitochondrial pathway was involved in the process of SPS induced apoptosis. *National Natural Science Foundation of China

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Zoladz, Phillip R., Monika Fleshner, and David M. Diamond. "Psychosocial animal model of PTSD produces a long-lasting traumatic memory, an increase in general anxiety and PTSD-like glucocorticoid abnormalities." Psychoneuroendocrinology 37, no. 9 (September 2012): 1531–45. http://dx.doi.org/10.1016/j.psyneuen.2012.02.007.

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Sela, Hagit, Hagit Cohen, Zeev Karpas, and Yehuda Zeiri. "Distinctive hippocampal zinc distribution patterns following stress exposure in an animal model of PTSD." Metallomics 9, no. 3 (2017): 323–33. http://dx.doi.org/10.1039/c6mt00207b.

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Matar, M. A., J. Zohar, and H. Cohen. "S.26.01 An innovative animal model of PTSD and its role in translational research." European Neuropsychopharmacology 20 (August 2010): S203. http://dx.doi.org/10.1016/s0924-977x(10)70227-3.

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Cohen, Hagit, Israel Liberzon, and Gal Richter-Levin. "Exposure to extreme stress impairs contextual odour discrimination in an animal model of PTSD." International Journal of Neuropsychopharmacology 12, no. 03 (August 13, 2008): 291. http://dx.doi.org/10.1017/s146114570800919x.

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HOFFMAN, JAY R., ISHAY OSTFELD, ZEEV KAPLAN, JOSEPH ZOHAR, and HAGIT COHEN. "Exercise Enhances the Behavioral Responses to Acute Stress in an Animal Model of PTSD." Medicine & Science in Sports & Exercise 47, no. 10 (October 2015): 2043–52. http://dx.doi.org/10.1249/mss.0000000000000642.

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DuWors, Robert, Peter Lang, James Derry, Peter Hoffman, Robert Wolford, Christopher Donovan-Dorval, and Jesse Capece. "Incarceration: An Unrecognized Public Health Crisis." CNS Spectrums 27, no. 2 (April 2022): 250–51. http://dx.doi.org/10.1017/s1092852922000621.

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AbstractBackgroundThe current study involved decades of research and a Systematic Literature Review.MethodsSix hundred and seventy-two former prisoners were interviewed, shortly upon release from incarceration. Multiple variables experienced while incarcerated were reviewed. Animal models around overcrowding and sustained levels of stress were also considered. The neurological underpinnings and relatedness to the concept of hypervigilance, thought to be an effective survival technique and PTSD were comprehensively researched. Hypervigilance is a well-regarded survival technique that is likened to the marine in a forward foxhole who hears a twig snap in the middle of the night and responds directly and decisively. The loading placed on the neuronal pathways and related brain regions is seen as a precursor to PTSD and otherwise burdensome to the overstimulated nervous system attempting to maintain an emotional equilibrium.ResultsA particular area of inquiry was around the presence of early parental/adult absence, recognized as a precursor to Complex PTSD (see World Health Organization ICD 11). But not delineated in DSM 5 (American Psychiatric Association). Significant rates of PTSD symptoms were identified in individuals experiencing early developmental trauma. All subjects met the criteria for Subthreshold PTSD at a minimum, and others (193) Posttraumatic Stress Disorder. Complex PTSD was descriptive of the findings of 179 of 193 subjects diagnosed with PTSD. These findings suggest that preexisting subthreshold Complex PTSD prior to incarceration predicts the development of Complex PTSD while incarcerated.ConclusionThe social cost of American Corrections incubates PTSD and subthreshold PTSD, releasing to society individuals more at risk to themselves and society than prior to the Correctional experience is incalculable. A philosophical reconsideration of the American Correctional experience at this time is long overdue. This philosophy is grounded on the concepts of Incapacitation; Punishment and Deterrence, v the European model generally of Rehabilitation and Reintegration.FundingNo funding

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Chang, Shao-Han, Ying Hao Yu, Alan He, Chen Yin Ou, Bai Chuang Shyu, and Andrew Chih Wei Huang. "BDNF Protein and BDNF mRNA Expression of the Medial Prefrontal Cortex, Amygdala, and Hippocampus during Situational Reminder in the PTSD Animal Model." Behavioural Neurology 2021 (March 8, 2021): 1–13. http://dx.doi.org/10.1155/2021/6657716.

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Whether BDNF protein and BDNF mRNA expression of the medial prefrontal cortex (mPFC; cingulated cortex area 1 (Cg1), prelimbic cortex (PrL), and infralimbic cortex (IL)), amygdala, and hippocampus (CA1, CA2, CA3, and dentate gyrus (DG)) was involved in fear of posttraumatic stress disorder (PTSD) during the situational reminder of traumatic memory remains uncertain. Footshock rats experienced an inescapable footshock (3 mA, 10 s), and later we have measured fear behavior for 2 min in the footshock environment on the situational reminder phase. In the final retrieval of situational reminder, BDNF protein and mRNA levels were measured. The results showed that higher BDNF expression occurred in the Cg1, PrL, and amygdala. Lower BDNF expression occurred in the IL, CA1, CA2, CA3, and DG. BDNF mRNA levels were higher in the mPFC and amygdala but lower in the hippocampus. The neural connection analysis showed that BDNF protein and BDNF mRNA exhibited weak connections among the mPFC, amygdala, and hippocampus during situational reminders. The present data did not support the previous viewpoint in neuroimaging research that the mPFC and hippocampus revealed hypoactivity and the amygdala exhibited hyperactivity for PTSD symptoms. These findings should be discussed with the previous evidence and provide clinical implications for PTSD.

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Radell, Milen L., Eid Abo Hamza, and Ahmed A. Moustafa. "Depression in post-traumatic stress disorder." Reviews in the Neurosciences 31, no. 7 (October 25, 2020): 703–22. http://dx.doi.org/10.1515/revneuro-2020-0006.

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AbstractMajor depressive disorder (MDD) symptoms commonly occur after trauma-exposure, both alone and in combination with post-traumatic stress disorder (PTSD). This article reviews recent research on comorbidity between these disorders, including its implications for symptom severity and response to treatment. Despite considerable symptom overlap, the two disorders represent distinct constructs and depend, at least in part, on separate biological mechanisms. Both, however, are also clearly related to stress psychopathology. We recommend that more research focus specifically on the study of individual differences in symptom expression in order to identify distinct subgroups of individuals and develop targeted treatments. However, a barrier to this line of inquiry is the trend of excluding particular patients from clinical trials of new interventions based on symptom severity or comorbidity. Another obstacle is the overreliance on self-report measures in human research. We argue that developing computer-based behavioral measures in order to supplement self-report can help address this challenge. Furthermore, we propose that these measures can help tie findings from human and non-human animal research. A number of paradigms have been used to model MDD-and PTSD-like behavior in animals. These models remain valuable for understanding the biological basis of these disorders in humans and for identifying potential interventions, but they have been underused for the study of comorbidity. Although the interpretation of animal behavior remains a concern, we propose that this can also be overcome through the development of close human analogs to animal paradigms.

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Sela, Hagit, Hagit Cohen, Zeev Karpas, and Yehuda Zeiri. "Correction: Distinctive hippocampal zinc distribution patterns following stress exposure in an animal model of PTSD." Metallomics 9, no. 5 (2017): 584. http://dx.doi.org/10.1039/c7mt90018j.

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Ronzoni, Giacomo, Alberto del Arco, Francisco Mora, and Gregorio Segovia. "Enhanced noradrenergic activity in the amygdala contributes to hyperarousal in an animal model of PTSD." Psychoneuroendocrinology 70 (August 2016): 1–9. http://dx.doi.org/10.1016/j.psyneuen.2016.04.018.

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Weiss, J. M., M. J. Ambrose, P. E. Simson, P. G. Simson, A. Webster, L. J. Hoffman, and V. Maljkovic. "Sleep disturbance induced by a sibgle stressful event in an animal model: relevance to PTSD?" Biological Psychiatry 35, no. 9 (May 1994): 710. http://dx.doi.org/10.1016/0006-3223(94)90998-9.

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Juven-Wetzler, Alzbeta, Hagit Cohen, Zeev Kaplan, Avi Kohen, Oren Porat, and Joseph Zohar. "Immediate ketamine treatment does not prevent posttraumatic stress responses in an animal model for PTSD." European Neuropsychopharmacology 24, no. 3 (March 2014): 469–79. http://dx.doi.org/10.1016/j.euroneuro.2013.08.007.

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Manjoch, Hadar, Ella Vainer, Michael Matar, Gal Ifergane, Joseph Zohar, Zeev Kaplan, and Hagit Cohen. "Predator-scent stress, ethanol consumption and the opioid system in an animal model of PTSD." Behavioural Brain Research 306 (June 2016): 91–105. http://dx.doi.org/10.1016/j.bbr.2016.03.009.

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Faturi, Claudia, Geielle Furtado, Sandra Mota-Ortiz, and Marcelo Mello. "151. Fear Extinction of Predatory Threat as an Animal Model of Posttraumatic Stress Disorder (PTSD)." Biological Psychiatry 81, no. 10 (May 2017): S63. http://dx.doi.org/10.1016/j.biopsych.2017.02.164.

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Luo, F. F., F. Han, and X. Y. Shi. "Changes of 5-HT1A receptor in the dorsal raphe nucleus in the rat model of Post-Traumatic Stress Disorder." European Psychiatry 26, S2 (March 2011): 1081. http://dx.doi.org/10.1016/s0924-9338(11)72786-9.

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IntroductionPosttraumatic stress disorder (PTSD) is characterized mainly by symptoms of reexperiencing, avoidance and hyperarousal as a consequence of catastrophic and traumatic events that are distinguished from ordinary stressful life events. Single-prolonged stress (SPS) is an established animal model for post-traumatic stress disorder (PTSD). The dorsal raphe nucleus (DR)-serotonin (5-HT) system is dramatically affected by swim stress and has been implicated in affective disorders. The 5-HT1A receptor (5-HT1AR) is critically involved in regulating mood and anxiety levels.ObjectiveIn this study, we investigated changes in the expression of 5-HT1AR in DR of rats after SPS which may reveal part of the pathogenesis of PTSD.MethodsRats were randomly divided into 24h, 4d and 7d groups after SPS and a normal control group, 5-HT1AR expression in DR was examined using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction.ResultsThe expression of 5-HT1AR in DR after SPS exposure was increased when compared to that in the control group (P < 0.05).ConclusionThese findings suggest increase of 5-HT1AR in DR of SPS rats, which may play important roles in the pathogenesis of PTSD rats.

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Vinay, Vidya Shree, Malathi S, and Ravindran R. "IMPAIRED OBJECT RECOGNITION MEMORY AND ACETYLCHOLINESTERASE ACTIVITY IN ANIMAL MODEL OF POST-TRAUMATIC STRESS DISORDER-RESTORED BY ECLIPTA ALBA LINN. A DIETARY HERB." Asian Journal of Pharmaceutical and Clinical Research 9, no. 9 (December 1, 2016): 117. http://dx.doi.org/10.22159/ajpcr.2016.v9s3.14190.

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ABSTRACTObjective: Acetylcholinesterase (AChE) inhibitors are important therapeutic targets to treat memory impairment caused due to stress, post-traumaticstress disorder (PTSD) results from traumatic stress exposure. Cognition and mood symptoms can begin or worsen after the traumatic event. In thisstudy, we aimed to evaluate the role of Eclipta alba Linn. as an antistressor, AChE inhibitor, and on object recognition memory in an animal model of PTSD.Methods: Adult male Wistar albino rats were randomly divided into four groups: Control, chronic unpredictable stress (CUS) (30 days), CUS+ethanolicextract of E. alba (EEEA) (200 mg/kg body weight), and EEEA (200 mg/kg body weight) treatment groups and were assessed for novel objectrecognition task (NORT), plasma corticosterone, and AChE activity.Results: We found significant improvement in NORT (p<0.05) plasma corticosterone levels in stress group was significantly increased (p<00.05)which is resumed with EEEA treatment (p<0.05) AChE activity was found to be reduced after EEEA treatment.Conclusion: EEEA is found to possess cognitive enhancing activity in the animal model of PTSD.Keywords: Recognition memory,PTSD,Unpredictable stress,Eclipta alba

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Nahum, Kesem, Doron Todder, Joseph Zohar, and Hagit Cohen. "The Role of Microglia in the (Mal)adaptive Response to Traumatic Experience in an Animal Model of PTSD." International Journal of Molecular Sciences 23, no. 13 (June 28, 2022): 7185. http://dx.doi.org/10.3390/ijms23137185.

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The present study investigates whether predator scent-stress (PSS) shifts the microglia from a quiescent to a chronically activated state and whether morphological alterations in microglial activation differ between individuals displaying resilient vs. vulnerable phenotypes. In addition, we examined the role that GC receptors play during PSS exposure in the impairment of microglial activation and thus in behavioral response. Adult male Sprague Dawley rats were exposed to PSS or sham-PSS for 15 min. Behaviors were assessed with the elevated plus-maze (EPM) and acoustic startle response (ASR) paradigms 7 days later. Localized brain expression of Iba-1 was assessed, visualized, and classified based on their morphology and stereological counted. Hydrocortisone and RU486 were administered systemically 10 min post PSS exposure and behavioral responses were measured on day 7 and hippocampal expression of Ionized calcium-binding adaptor molecule 1 (Iba-1) was subsequently evaluated. Animals whose behavior was extremely disrupted (PTSD-phenotype) selectively displayed excessive expression of Iba-1 with concomitant downregulation in the expression of CX3C chemokine receptor 1 (CX3CR1) in hippocampal structures as compared with rats whose behavior was minimally or partially disrupted. Changes in microglial morphology have also been related only to the PTSD-phenotype group. These data indicate that PSS-induced microglia activation in the hippocampus serves as a critical mechanistic link between the HPA-axis and PSS-induced impairment in behavioral responses.

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Brand, Sarel Jacobus, and Brian Herbert Harvey. "Exploring a post-traumatic stress disorder paradigm in Flinders sensitive line rats to model treatment-resistant depression II: response to antidepressant augmentation strategies." Acta Neuropsychiatrica 29, no. 4 (October 3, 2016): 207–21. http://dx.doi.org/10.1017/neu.2016.50.

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ObjectivePost-traumatic stress disorder (PTSD) displays high co-morbidity with major depression and treatment-resistant depression (TRD). Earlier work demonstrated exaggerated depressive-like symptoms in a gene×environment model of TRD and an abrogated response to imipramine. We extended the investigation by studying the behavioural and monoaminergic response to multiple antidepressants, viz. venlafaxine and ketamine with/without imipramine.MethodsMale Flinders sensitive line (FSL) rats, a genetic model of depression, were exposed to a time-dependent sensitisation (TDS) model of PTSD and compared with stress naive controls. 7 days after the TDS procedures, immobility and coping (swimming and climbing), behaviours in the forced swim test (FST) as well as hippocampal and cortical 5-hydroxyindoleacetic acid (5HIAA) and noradrenaline (NA) levels were analysed. Response to imipramine, venlafaxine and ketamine treatment (all 10 mg/kg×7 days) alone and in combination were subsequently studied.ResultsTDS exacerbated depressive-like behaviour of FSL rats in the FST. Imipramine, venlafaxine and ketamine were ineffective as monotherapy in TDS-exposed FSL rats. However, combining imipramine with either venlafaxine or ketamine resulted in significant anti-immobility effects and enhanced coping behaviours. Only ketamine+imipramine (frontal-cortical 5HIAA and NA), ketamine alone (frontal-cortical and hippocampal NA) and venlafaxine+imipramine (frontal-cortical NA) altered monoamine responses versus untreated TDS-exposed FSL rats.ConclusionExposure of FSL rats to TDS inhibits antidepressant response at behavioural and neurochemical levels. Congruent with TRD, imipramine plus venlafaxine or ketamine overcame treatment resistance in these animals. These data further support the hypothesis that exposure of FSL rats to a PTSD-like paradigm produces a valid animal model of TRD and warrants further investigation.

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Wang, Sheng-Chiang, Chen-Cheng Lin, Chun-Chuan Chen, Nian-Sheng Tzeng, and Yia-Ping Liu. "Effects of Oxytocin on Fear Memory and Neuroinflammation in a Rodent Model of Posttraumatic Stress Disorder." International Journal of Molecular Sciences 19, no. 12 (December 3, 2018): 3848. http://dx.doi.org/10.3390/ijms19123848.

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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 IL-1β, IFN-γ, and TNF-α 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, IL-1β and IFN-γ 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.

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Ebenezer, Philip J., C. Brad Wilson, Leslie D. Wilson, Anand R. Nair, and Francis J. "The Anti-Inflammatory Effects of Blueberries in an Animal Model of Post-Traumatic Stress Disorder (PTSD)." PLOS ONE 11, no. 9 (September 7, 2016): e0160923. http://dx.doi.org/10.1371/journal.pone.0160923.

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Groer, M., S. Wolfe, C. R. Park, B. Kupchak, J. Volek, and D. M. Diamond. "68. Reduction of hair glucocorticoid levels in an animal model of post-traumatic stress disorder (PTSD)." Brain, Behavior, and Immunity 32 (September 2013): e20. http://dx.doi.org/10.1016/j.bbi.2013.07.080.

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Oosthuizen, Frasia, Gregers Wegener, and Brian H. Harvey. "Nitric oxide as inflammatory mediator in post-traumatic stress disorder (PTSD): evidence from an animal model." Neuropsychiatric Disease and Treatment 1, no. 2 (2005): 109–23. http://dx.doi.org/10.2147/nedt.1.2.109.61049.

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Hoffman, Jay R., Ishay Ostfeld, Jeffrey R. Stout, Roger C. Harris, Zeev Kaplan, and Hagit Cohen. "β-Alanine supplemented diets enhance behavioral resilience to stress exposure in an animal model of PTSD." Amino Acids 47, no. 6 (March 11, 2015): 1247–57. http://dx.doi.org/10.1007/s00726-015-1952-y.

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Koresh, Ori, Zeev Kaplan, Joseph Zohar, Michael A. Matar, Amir B. Geva, and Hagit Cohen. "Distinctive cardiac autonomic dysfunction following stress exposure in both sexes in an animal model of PTSD." Behavioural Brain Research 308 (July 2016): 128–42. http://dx.doi.org/10.1016/j.bbr.2016.04.024.

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Gałązka, Małgorzata, Dariusz Soszyński, and Katarzyna Dmitruk. "Neurobiological fundamentals of posttrumatic stress disorder – a possible role of circadian rhythms deregulations." Postępy Higieny i Medycyny Doświadczalnej 72 (May 17, 2018): 406–16. http://dx.doi.org/10.5604/01.3001.0012.0537.

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Posttraumatic stress disorder is a complex anxiety disorder induced by a stress factor. It is believed that this fear conditioning impairment may be crucial to PTSD development. Stress induced electrophysiological and neurohormonal changes within the hippocampus, amygdala, prefrontal cortex or locus coeruleus may impair other regional functions of the central nervous system like suprachiasmatic nuclei functions. Furthermore, the activation of llocus coeruleus or its impact on the activity of superchiasmatic nuclei may influence the circadian rhythm. The influence of stress factor on the hypothalamus – pituitary – adrenal gland axis (HPA) activity is well documented. Also PTSD accompanied changes of the HPA axis are well known. Unfortunately, due to methodological problems, the evaluation of stress induced HPA axis circadian rhythm changes is limited. Another physiological parameter, characterised by circadian rhythm is body temperature. Stress factor exposure induced a strong decrease in the daily rhythm amplitude during day/night cycles in the animal model of PTSD. Described disturbances to the rhythm was suprachiasmatic nuclei activity independent.

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Laukova, Marcela, Lishay G. Alaluf, Lidia I. Serova, Victoria Arango, and Esther L. Sabban. "Early Intervention With Intranasal NPY Prevents Single Prolonged Stress-Triggered Impairments in Hypothalamus and Ventral Hippocampus in Male Rats." Endocrinology 155, no. 10 (October 1, 2014): 3920–33. http://dx.doi.org/10.1210/en.2014-1192.

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Abstract Intranasal administration of neuropeptide Y (NPY) is a promising treatment strategy to reduce traumatic stress-induced neuropsychiatric symptoms of posttraumatic stress disorder (PTSD). We evaluated the potential of intranasal NPY to prevent dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, a core neuroendocrine feature of PTSD. Rats were exposed to single prolonged stress (SPS), a PTSD animal model, and infused intranasally with vehicle or NPY immediately after SPS stressors. After 7 days undisturbed, hypothalamus and hippocampus, 2 structures regulating the HPA axis activity, were examined for changes in glucocorticoid receptor (GR) and CRH expression. Plasma ACTH and corticosterone, and hypothalamic CRH mRNA, were significantly higher in the vehicle but not NPY-treated group, compared with unstressed controls. Although total GR levels were not altered in hypothalamus, a significant decrease of GR phosphorylated on Ser232 and increased FK506-binding protein 5 mRNA were observed with the vehicle but not in animals infused with intranasal NPY. In contrast, in the ventral hippocampus, only vehicle-treated animals demonstrated elevated GR protein expression and increased GR phosphorylation on Ser232, specifically in the nuclear fraction. Additionally, SPS-induced increase of CRH mRNA in the ventral hippocampus was accompanied by apparent decrease of CRH peptide particularly in the CA3 subfield, both prevented by NPY. The results show that early intervention with intranasal NPY can prevent traumatic stress-triggered dysregulation of the HPA axis likely by restoring HPA axis proper negative feedback inhibition via GR. Thus, intranasal NPY has a potential as a noninvasive therapy to prevent negative effects of traumatic stress.

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