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Статті в журналах з теми "PTSD animal model"
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.
Повний текст джерелаPerez-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.
Повний текст джерелаZhan, 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.
Повний текст джерелаCohen, 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.
Повний текст джерелаCohen, 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.
Повний текст джерелаLiberzon, 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.
Повний текст джерелаStarcevic, 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.
Повний текст джерелаBrand, 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.
Повний текст джерелаJia, 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.
Повний текст джерелаHashimoto, 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.
Повний текст джерелаДисертації з теми "PTSD animal model"
Malan-Muller, Stefanie. "Molecular mechanisms of D-cycloserine in a fear extinction posttraumatic stress disorder (PTSD) animal model." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86714.
Повний текст джерелаENGLISH ABSTRACT: Posttraumatic stress disorder (PTSD) is a severe, chronic and debilitating psychiatric disorder that can present after the experience of a life-threatening traumatic event. D-cycloserine (DCS), a partial N-methyl-D-aspartate (NMDA) receptor agonist, has been found to augment cognitive behavioural therapy by facilitating fear extinction; however, the precise mechanisms whereby DCS ameliorates fear triggered by a traumatic context remains to be fully elucidated. This study aimed to (i) identify the molecular mechanisms of intrahippocampally administered DCS in facilitating fear extinction in a rat model of PTSD by investigating gene expression profiles in the left dorsal hippocampus (LDH) of male Sprague Dawley rats and (ii) determine whether microRNA (miRNA) expression and DNA methylation mediated these gene expression changes. An adapted version of the PTSD animal model described by Siegmund and Wotjak (2007) was utilised. The total number of 120 rats were grouped into four experimental groups (of 30 rats per group) based on fear conditioning and the intrahippocampal administration of either DCS or saline: (1) fear conditioned + intrahippocampal saline administration (FS), (2) fear conditioned + intrahippocampal DCS administration (FD), (3) control + intrahippocampal saline administration (CS) and (4) control + intrahippocampal DCS administration (CD). Behavioural tests (the light/dark [L/D] avoidance test, forced swim test and open field test) were conducted to assess anxiety and PTSD-like behaviours. The L/D avoidance test was the most sensitive behavioural test of anxiety and was subsequently used to differentiate maladapted (animals that displayed anxiety-like behaviour) and well-adapted (animals that did not display anxiety-like behaviour) subgroups. In order to identify genes that were differentially expressed between FS maladapted (FSM) (n = 6) vs. FD well-adapted (FDW) (n = 6) groups, RNA sequencing was performed on the Illumina HiSeq 2000 which generated more than 60 million reads per sample. This was followed by subsequent bioinformatics analyses (using the software programs TopHat, Bowtie, Cuffdiff and Bio-Ontological Relationship Graph (BORG) database (that identifies genes that may be biologically relevant) to identify biologically relevant differentially expressed genes between the treatment groups. Epigenetic mechanisms mediating observed differences in gene expression were investigated by conducting DNA methylation and miRNAseq analyses in the FDW and FSM experimental groups. DNA methylation was investigated using real-time quantitative PCR (qPCR) amplification followed by high resolution melt analysis on the Rotor-GeneTM 6000. Differences in miRNA expression levels between the FDW and FSM groups were investigated by sequencing the miRNA fraction on the MiSeq platform. The bioinformatics pipeline used to analyse the RNAseq data identified 93 genes that were significantly downregulated in the FDW group compared to the FSM group. Forty-two of these genes were predicted to be biologically relevant (based on BORG analysis). Integrative network analyses revealed subsets of differentially expressed genes common across biological functions, pathways and disorders. The co-administration of DCS and behavioural fear extinction downregulated immune system genes and genes that transcribe proinflammatory and oxidative stress molecules. These molecules mediate neuroinflammation and subsequently cause neuronal damage. DCS also regulated genes involved in learning and memory processes. Additionally, a subset of the genes, which have been found to be associated with disorders that commonly co-occur with PTSD (such as cardiovascular disease, metabolic disease, Alzheimer‘s and Parkinson‘s disease), was downregulated by the co-administration of DCS and behavioural fear extinction. In order to determine whether real-time qPCR analysis would be sensitive enough to detect differential expression in those genes found to be differentially expressed in RNAseq analysis, the expression of nine genes was analysed using SYBR Green qPCR technology. In the LDH, six of the nine genes were found to be differentially expressed between FDW and FSM groups and one gene, matrix metallopeptidase 9 (MMP9), was observed to be differentially expressed between these two groups in the blood. Three of the nine genes for which differential expression levels were investigated using SYBR Green real-time qPCR, contained CpG islands and were used for CpG island DNA methylation analysis. Results indicated that CpG island DNA methylation did not mediate differential gene expression of TRH, NPY or MT2A. Bioinformatics analysis of miRNAseq data identified 23 miRNAs that were differentially expressed between the FDW and FSM groups. Several of these miRNAs have previously been found to be involved in brain development and behavioural measures of anxiety. Furthermore, functional luciferase analysis indicated that the upregulation of rno-mi31a-5p could have facilitated the downregulation of interleukin 1 receptor antagonist gene (IL1RN) as detected in RNAseq. RNAseq and miRNAseq analyses in this PTSD animal model identified differentially expressed genes and miRNAs that serve to broaden our understanding of the mechanism whereby DCS facilitates fear extinction. To this end, immune system genes and genes transcribing proinflammatory and oxidative stress molecules were among the genes that were found to be differentially expressed between the FDW and FSM groups. Based on the results obtained, it can be hypothesised that DCS attenuates neuroinflammation and subsequent neuronal damage, and also regulates genes involved in learning and memory processes. Concomitantly, these gene expression alterations mediate optimal neuronal functioning, plasticity, learning and memory (such as fear extinction memory) which contribute to the fear extinction process. Furthermore, biologically relevant differentially expressed genes that were associated with DCS facilitation of fear extinction and with other chronic medical conditions, such as cardiovascular disease and metabolic diseases, might help to explain the co-occurrence of these disorders with PTSD. In conclusion, Identifying the molecular underpinnings of DCS-mediated fear extinction brings us closer to understanding the process of fear extinction and could, in future work be used to explore novel therapeutic targets to effectively treat PTSD and related disorders.
AFRIKAANSE OPSOMMING: Posttraumatiese stressindroom is 'n ernstige, kroniese aftakelende psigiatriese toestand wat kan ontwikkel na 'n lewensgevaarlike traumatiese gebeurtenis. Daar is bevind dat die gesamentlike toediening van D-sikloserien (DCS), 'n N-metiel-D-aspartaat (NMDA) reseptor agonis, en kognitiewe gedragsterapie effektief is in die bemiddeling van vrees uitwissing; maar die presiese meganisme waar deur DCS die vrees wat deur 'n traumatiese konteks ontlok word verminder, is egter onduidelik. Hierdie studie het beoog om (i) die molekulêre meganismes te identifiseer waardeur intra-hippokampaal toegediende DCS vrees uitwissing fasiliteer, in 'n rot model van posttraumatiese stressindroom, deur geen uitdrukkingsprofiele in the linker dorsale hippokampus (LDH) van manlike Sprague Dawley rotte te ondersoek en (ii) om te bepaal of mikroRNA (miRNA) uitdrukking en DNA metilering die veranderinge in geen uitdrukking bemiddel het. 'n Gewysigde weergawe van die posttraumatiese stressindroom diere model, beskryf deur Siegmund en Wotjak (2007), was gebruik tydens die studie. Rotte was in vier groepe verdeel, vrees kondisionering + soutwater (FS), vrees kondisionering + DCS (FD), kontrole + soutwater (CS) en kontrole + DCS (CD). Gedragstoetse was uitgevoer om angstige, vreesvolle en posttraumatiese stressindroom-tipe gedrag te evalueer. Gedurende die lig/donker (L/D) vermydingstoets het die FS groep aansienlik meer tyd in die donker kompartement deurgebring ('n indikasie van vreesvolle gedrag) in vergelyking met die CS en die FD groepe wat meer tyd in die verligte kompartement deurgebring het ('n indikasie van vreeslose gedrag). Die L/D toets was die mees sensitiewe gedragstoets vir angstige en vreesvolle gedrag en was gevolglik gebruik om die diere te sub-groepeer in wanaangepaste (diere wat angstige en vreesvolle gedrag vertoon het) en goedaangepaste (diere wat nie angstige en vreesvolle gedrag vertoon het nie) subgroepe. Nuwe generasie RNA volgordebepaling (RNAseq) van die LDH RNA en daaropvolgende bioinformatiese analise was uitgevoer om gene te identifiseer wat differensieel uitgedruk is tussen die twee behandelingsgroepe van belang in die betrokke studie, naamlik FS wanaangepaste (FSM) teenoor FD goedaangepaste (FDW) groepe. Epigenetiese analises was uitgevoer om te bepaal of differensieel uitgedrukte miRNAs of CpG-eiland DNA metilasie die differensiële geenuitdrukking bemiddel het. Bioinformatiese analises van die RNAseq data het 93 gene geïdentifiseer waarvan die geen uitdrukking beduidend onderdruk was in die FDW groep in vergelyking met die FSM groep; 42 van hierdie gene was voorspel om biologies relevant te wees. Geïntegreerde netwerk analise het onthul dat sekere van die differensieel uitgedrukte gene gemeenskaplik was tussen verskeie biologiese funksies, padweë en versteurings. DCS het die uitdrukking van immuun-sisteem gene en pro-inflammatoriese en oksidatiewe stres gene verlaag. Hierdie molekules medieer neuro-inflammasie wat gevolglik tot neurale skade lei. DCS het ook gene gereguleer wat betrokke is by leer en geheue prosesse. DCS het onder meer ook die geenuitdrukking verlaag van 'n sub-groep van gene wat voorheen geassosier is met komorbiede versteurings van PTSD. SYBR Green real-time qPCR (werklike tyd kwantitatiewe polimerase ketting reaksie) analise was ondersoek om te bepaal of hierdie metode sensitief genoeg sou wees om die verlaagde geen-uitdrukking van verskeie van die biologies relevante differensieel uitgedrukte gene te identifiseer, in dieselfde LDH komplementêre DNA (cDNA) monsters as wat in die RNAseq gebruik is, asook in die bloed cDNA monsters. SYBR Green real-time qPCR was in staat om ses, van die nege, differensieel uitgedrukte gene in die LDH cDNA monsters en een geen, matriks metallopeptidase 9 (MMP9), in die bloed cDNA monsters op te tel. Drie van die gene waarvoor SYBR Green real-time qPCR gebruik is om differensiële geenuitdrukking te toets, het CpG eilande bevat en was gevolglik gebruik in CpG eiland DNA metilering analises. Resultate het getoon dat CpG eiland DNA metilering nie die differensiële geenuitdrukking van TRH, NPY of MT2A gedryf het nie. Bioinformatiese analises van die miRNAseq data het 23 miRNAs geïdentifiseer wat differensieël uitgedruk was tussen die FDW en FSM groepe. Verskeie van hierdie miRNAs is reeds voorheen beskryf om betrokke te wees in brein ontwikkeling en angs gedrags metings. Funksionele luciferase analises het verder aangedui dat die verhoogde uitdrukking van rno-mi31a-5p moontlik die verlaagde geen uitdrukking van IL1RN, soos waargeneem in die RNAseq data, kon bewerkstellig het. RNAseq en miRNAseq analises in hierdie posttraumatiese stressindroom dieremodel het differensieël uitgedrukte gene en miRNAs geïdentifiseer wat dien om die verstaanswyse te verbreed van hoe DCS die vrees uitwissings proses fasiliteer. Die meganismes waardeur DCS vrees uitwissings bewerkstellig het sluit die verlaging van immuun-sisteem geen-uitdrukking in, sowel as verlaagde uitdrukking van gene wat pro-inflammatoriese en oksidatiewe stress gene transkribeer. DCS het daardeur neuro-inflammasie en gevolglike neurale skade voorkom. DCS het daarmee saam ook gene gereguleer wat betrokke is by leer en geheue prosesse. Hierdie gesamentlike veranderings in geen uitdrukking het gelei tot die uiteindelike bewerkstelling van optimale neurale funksionering, plastisiteit, leer en geheue prosesse wat uiteindelik bygedra het tot vrees uitwissing. Biologies relevante differensieël uitgedrukte gene wat ook geassosieer was met ander kondisies, soos middel verwante versteurings en metaboliese versteurings, kan help om die komorbiditeit met posttraumatiese stressindroom te verklaar. Identifisering van die molekulêre grondslae van DCS bemiddelde vrees uitwissing verbreed ons begrip en verstaan van vrees uitwissing en kan moontlik, in toekomstige navorsing gebruik word om nuwe innoverende terapeutiese teikens te verken om sodoende posttraumatiese stressindroom meer effektief te kan behandel.
Enman, Nicole Marie. "Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/259963.
Повний текст джерелаPh.D.
Posttraumatic stress disorder (PTSD) co-occurs with substance use disorders at high rates, but the neurobiological basis of this relationship remains largely unknown. Identifying mechanisms that underlie this association is necessary, and recognizing pathologies shared by these disorders may provide pertinent information in understanding their functional relationship. Separate lines of evidence suggest that PTSD and drug addiction may share a common feature, that is, dysregulation of the brain's reward circuitry. We hypothesize that PTSD results in reduced dopaminergic neurotransmission which may contribute to deficient reward function and vulnerability to drug-seeking behavior. To address this hypothesis, we combined single-prolonged stress (SPS), a rodent model of PTSD, with a series of behavioral and neuropharmacological assays to assess dopaminergic reward function and cocaine intake. The results of the studies presented herein extend our understanding of the effects of severe stress on drug reinforcement and consumption, and establish a potential mechanism by which PTSD produces deficient reward function through alterations in the dopamine system. A modified SPS procedure consisting of 2 hours of restraint, 20 minutes of group swimming, isoflurane exposure until loss consciousness, and 7 days of isolation was used to induce severe stress in our studies. Initial studies were conducted to examine the effect of SPS on cocaine-conditioned reward and anhedonia-like behavior in adult male Sprague-Dawley rats. Using a biased conditioned place preference paradigm, unstressed controls demonstrated a significant preference for the cocaine-paired context following four pairings with cocaine (5-20 mg/kg, i.p.). Preference for the cocaine-paired side was significantly lower in rats exposed to SPS, suggesting a deficit in the rewarding properties of cocaine following exposure to severe stress. Anhedonia-like behavior was assessed by a two-bottle choice sucrose preference test. Robust consumption of sucrose solution (0.25-1%) was observed in rats that underwent control handling, however, SPS significantly reduced sucrose intake compared to controls. These results suggest an increase in anhedonia-like behavior or a reduction in the rewarding effects of sucrose as a non-drug reinforcer. Finally, basal behavioral activity in SPS rats was compared to unstressed controls in a 24-hour test. Results indicate a significant reduction in spontaneous nocturnal activity following SPS versus control handling. In contrast, hyperlocomotion induced by an acute cocaine injection (5-20 mg/kg, i.p.) was unaltered between rats that underwent SPS or control handling. These data suggest that deficient behavioral activity may be specific to voluntary movements or behavior, and support an increase in anhedonia following exposure to SPS. Intravenous cocaine self-administration was conducted to examine the effect of SPS on the acquisition, motivation, and escalation of cocaine intake. Acquisition of cocaine self-administration was studied using an escalating dose regimen in which rats had sequential access to 0.1875, 0.375, and 0.75 mg/kg/infusion on a fixed-ratio 1 schedule of reinforcement. Rats exposed to SPS did not significantly differ from control handled animals in the latency to meet acquisition criteria (consumption of 6.75 mg/kg/day for 3 consecutive days) or the general pattern and level of cocaine intake at each dose. A subsequent study assessing the breakpoint for cocaine self-administration using a progressive-ratio schedule of reinforcement determined a dose-dependent increase in motivation to work for cocaine (0-1.5 mg/kg/infusion) across both experimental groups. However, motivation to obtain cocaine was similar between SPS and unstressed rats, as there was no significant difference in breakpoint for cocaine self-administration at any dose of cocaine tested. To evaluate potential differences in the transition to escalated cocaine intake, self-administration was measured using an extended-access procedure in which unlimited cocaine (0.375 mg/kg/infusion) was available for six hours daily. Upon extended-access to cocaine, SPS significantly attenuated cocaine intake compared to control handling over 14 sessions. Despite a significant reduction in cocaine intake, rats exposed to SPS still significantly escalated their cocaine intake over the course of 14 days. These results suggest that escalation of cocaine intake occurred in the presence of lower total doses of cocaine in the SPS exposed animals compared to controls. In addition, SPS rats demonstrated a greater percent increase in cocaine consumption compared to controls. This finding suggests that rats exposed to SPS compensated for a decrease in cocaine reinforcement by escalating their intake to a greater magnitude than controls. These studies indicate that SPS may not alter the acquisition of cocaine self-administration or motivation for cocaine. However, the finding of reduced cocaine intake upon extended-access in SPS rats is consistent with a deficit in cocaine-induced reward. The ability of SPS rats to escalate cocaine intake in the presence of less cocaine, or a greater magnitude of escalated cocaine intake than controls, may reflect mechanisms leading to enhanced vulnerability to cocaine abuse. To understand the mechanisms of reduced reward and behavior in the SPS model of PTSD, a series of neurochemical assays was used to assess the ability of SPS to induce dysfunction of dopaminergic neurotransmission. Using high performance liquid chromatography, tissue levels of dopamine and the dopamine metabolites DOPAC and HVA were measured immediately and one week following SPS or control handling. Tissue obtained from SPS rats demonstrated significant decreases in dopamine, DOPAC, and HVA content in both the nucleus accumbens and caudate putamen immediately following SPS and one week later, suggesting a potential deficit in dopaminergic tone. Quantitative autoradiography was used measure the density of dopamine transporters and dopamine D1 and D2 receptors. [3H]WIN35428 binding to dopamine transporters was higher in the nucleus accumbens of SPS rats compared to controls, suggesting an increase in dopamine transporter density following severe stress. The level of [3H]WIN35428 binding in the caudate putamen was not different between groups. [3H]Raclopride binding to D2 receptors was significantly reduced in both the nucleus accumbens and caudate putamen following SPS versus control handling. These results suggest a decrease in the density of striatal D2 receptors. D1 receptor expression was not significantly altered by SPS, as no significant difference in [3H]SCH23390 binding was detected in SPS rats compared to controls. A preliminary functional assessment of dopamine transporters revealed a significant increase in dopamine uptake in the nucleus accumbens of SPS rats compared to controls, whereas uptake in the caudate putamen was unaltered between groups. Enhanced dopamine uptake following SPS is consistent with the increase in dopamine transporter density observed in the nucleus accumbens of SPS rats. Activation of D1 receptors and G-protein mediated transduction was assessed using an adenylyl cyclase assay with the D1 agonist SKF82958. In the caudate putamen, a significant decrease in D1 receptor-stimulated cAMP production was revealed in SPS rats compared to controls, whereas SKF82958-induced cAMP was unchanged in the nucleus accumbens. Finally, the function of D2 dopamine receptors was assessed by D2 receptor-stimulated [35S]GTPγS binding using quinpirole. In the caudate putamen, [35S]GTPγS binding following stimulation of D2 receptors was enhanced by SPS compared to control handling, whereas no difference was observed between groups in the nucleus accumbens. These results indicate increased D2 receptor-mediated activation of G-proteins in the caudate putamen following SPS. In summary, the studies described herein tested the hypothesis that reduced dopaminergic function may be a mechanism for deficient reward and heightened susceptibility to drug use in PTSD. Results demonstrated a significant reduction in cocaine-conditioned reward, as well as attenuated sucrose preference and spontaneous activity in rats exposed to SPS. These findings are consistent with the presence of a dysfunctional reward system which may contribute to anhedonia-like behavior in PTSD. Furthermore, reward deficits may promote altered patterns of cocaine taking behavior and vulnerability to substance abuse. Results demonstrated significant escalation of drug intake following exposure to SPS, which occurred in the presence of less cocaine than controls. A greater increase in cocaine intake was observed in SPS rats over the course of escalation, which may reflect a mechanism for enhanced vulnerability to the development of a substance use disorder in PTSD. Dopaminergic dysfunction may contribute to deficient reward capacity and an altered pattern of cocaine intake in SPS. SPS-induced alterations in dopamine function included a reduction in striatal dopamine content alongside enhanced dopamine transporter levels and function. Mild alterations in D2 receptor density and the function of D1 and D2 receptors were also observed. These findings support the hypothesis that PTSD results in reduced dopaminergic neurotransmission, which may contribute to deficient reward function and altered drug-seeking behavior. Identifying the pathology of PTSD, such as altered dopamine neurotransmission, may lead to enhanced treatment strategies and interventions to prevent substance abuse in persons with PTSD.
Temple University--Theses
Hamlyn, Eugene. "Investigating the role of AMPAkines in an animal model of post-traumatic stress disorder (PTSD) / Eugene Hamlyn." Thesis, North-West University, 2008. http://hdl.handle.net/10394/3718.
Повний текст джерелаThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2009.
Bothma, Tanya. "Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma." Thesis, North-West University, 2004. http://hdl.handle.net/10394/477.
Повний текст джерелаThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.
Myburgh, Jacolene. "A pharmacokinetic-pharmacodynamic relationship study between GABA-ergic drugs and anxiety levels in an animal model of PTSD / Jacolene Myburgh." Thesis, North-West University, 2005. http://hdl.handle.net/10394/1320.
Повний текст джерелаJeeva, Zakkiyya Igbal. "The role of monoamines in post traumatic stress disorder (PTSD) using a time dependent sensitization animal model / Zakkiyya Igbal Jeeva." Thesis, North-West University, 2004. http://hdl.handle.net/10394/587.
Повний текст джерелаThesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2005.
Seetharaman, Shyam. "The influence of daily social stimulation in ameliorating PTSD-like behavioral and physiological changes in rats exposed to chronic psychosocial stress." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0003258.
Повний текст джерелаZoladz, Phillip R. "An Ethologically Relevant Animal Model of Post-Traumatic Stress Disorder: Physiological, Pharmacological and Behavioral Sequelae in Rats Exposed to Predator Stress and Social Instability." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002688.
Повний текст джерелаChEN, CHANG-HAO, and 陳張豪. "Investigate the Effects of Environmental Enrichment for Post Traumatic Stress Disorder (PTSD) in Animal Model." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/89363146198848383011.
Повний текст джерела國防醫學院
生物及解剖學研究所
104
Post-traumatic stress disorder (PTSD) is a complex disease that is defined by individual experience to intense, life-threatening trauma then lead to various physical and psychological abnormalities. The re-experiencing and avoidance symptoms of the disorder may hinder daily life in PTSD patients, and they develop additional debilitating symptoms, including persistent anxiety, exaggerated startle, and cognitive impairments. Environmental enrichment has been showed to enhance learning and memory, improve neurological diseases and anxiety behavior. Furthermore, previous research also found that estrogen may correlate with the stress response. In the present study, we want to investigate the effects of environmental enrichment on anxiety and depress behavior before or after survival stress in male rats. Furthermore, the concentrations of estradiol during experiments were detected. In this study, we breed rats in different environment and observe the effect of PTSD related symptoms. Therefore we use eight-week-old SD male rats expose to survival pressure, and then divided into three groups: control, isolate feeding (ISO) and enrich environment (EE). We use the behavioral tests (open field test and tail suspension test) to determine the level of anxiety and depress in animals. Serum samples of all animals were also collected through tail vein for hormone analysis (estrogen) before and after survival stress. From our results in tail suspension test and open field test, the animals of EE before stress and Continue EE could resistant to stress. However, the group of Continue ISO showed more depress in tail suspension test. On the other hand, the group of EE before stress showed more anxiety in open field test. In the results of hormone test, we found survival stress enhances E2 level in male rats, and animals of EE group in second bitch showed less enhanced. Therefore, our result showed enhanced anxiety, depress and serum estradiol levels after survival stress. Environmental enrichment could constant these change. Finally, we purpose environmental enrichment may be one of the improved ways for PTSD.
Wu, Hsueh-Fu, and 吳學府. "The Anxiolytic-like Effects Of Taiwanese Green Propolis (TGP) By PTSD Animal Model And CRMP1 Regulates Consolidation Of Contextual Fear Memory." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/curqu7.
Повний текст джерелаКниги з теми "PTSD animal model"
Perkins, Elizabeth C., Shaun P. Brothers, and Charles B. Nemeroff. Animal Models for Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0024.
Повний текст джерелаMilad, Mohammed R., and Kylie N. Moore. Neurobiology and Neuroimaging of PTSD. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0015.
Повний текст джерелаMorinobu, Shigeru, Shigeto Yamamoto, and Manabu Fuchikami. Translational Research from Animals to Humans. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0017.
Повний текст джерелаDunsmoor, Joseph E., and Rony Paz. Generalization of Learned Fear. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0004.
Повний текст джерелаHowlett, Jonathon R., and Murray B. Stein. Novel Prevention and Treatment Approaches to PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0021.
Повний текст джерелаTobia, Anna. Integrative Treatment of Emotional Traumas. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0020.
Повний текст джерелаCohen, Hagit, and Joseph Zohar. The Role of Glucocorticoids in the (Mal)adaptive Response to Traumatic Experience. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0038.
Повний текст джерелаKarpova, Nina N. Pharmacological Adjuncts and Evidence-Supported Treatments for Trauma. Edited by Sara Maltzman. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199739134.013.32.
Повний текст джерелаЧастини книг з теми "PTSD animal model"
Gal, Richter-Levin, Kehat Orli, Limor Shtoots, and Anunu Ruchi. "Challenge of Developing a Validated Animal Model of PTSD: Focus on Juvenile Stress Model." In Comprehensive Guide to Post-Traumatic Stress Disorders, 1515–29. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-08359-9_121.
Повний текст джерелаGal, Richter-Levin, Kehat Orli, Limor Shtoots, and Anunu Ruchi. "Challenge of Developing a Validated Animal Model of PTSD – Focus on Juvenile Stress Model." In Comprehensive Guide to Post-Traumatic Stress Disorder, 1–12. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-08613-2_121-1.
Повний текст джерелаCohen, Shlomi, Michael A. Matar, Joseph Zohar, and Hagit Cohen. "Brain Pathways of Traumatic Memory: Evidence from an Animal Model of PTSD." In Sleep and Combat-Related Post Traumatic Stress Disorder, 127–43. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7148-0_11.
Повний текст джерелаChakraborty, Nabarun, James Meyerhoff, Marti Jett, and Rasha Hammamieh. "Genome to Phenome: A Systems Biology Approach to PTSD Using an Animal Model." In Methods in Molecular Biology, 117–54. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6952-4_6.
Повний текст джерелаZoladz, Phillip R., and David M. Diamond. "Psychosocial Stress in Rats: Animal Model of PTSD Based on Clinically Relevant Risk Factors." In Comprehensive Guide to Post-Traumatic Stress Disorders, 1531–51. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-08359-9_58.
Повний текст джерелаZoladz, Phillip R., and David M. Diamond. "Psychosocial Stress in Rats: Animal Model of PTSD Based on Clinically Relevant Risk Factors." In Comprehensive Guide to Post-Traumatic Stress Disorder, 1–17. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-08613-2_58-1.
Повний текст джерелаMacCallum, Phillip, Jesse Whiteman, Therese Kenny, Katelyn Fallon, Sriya Bhattacharya, James Drover, and Jacqueline Blundell. "Developing a Reliable Animal Model of PTSD in Order to Test Potential Pharmacological Treatments." In Handbook of Posttraumatic Stress, 373–402. New York: Routledge, 2021. http://dx.doi.org/10.4324/9781351134637-18.
Повний текст джерелаCain, Christopher, and Regina Sullivan. "Amygdala contributions to fear and safety conditioning: insights into PTSD from an animal model across development." In Posttraumatic Stress Disorder, 81–104. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118356142.ch4.
Повний текст джерелаWilkinson, Courtney, Harrison Blount, Lori Knackstedt, and Marek Schwendt. "Investigation of Individual Differences in Stress Susceptibility and Drug-Seeking in an Animal Model of SUD/PTSD Comorbidity." In Methods for Preclinical Research in Addiction, 247–64. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1748-9_10.
Повний текст джерелаFlandreau, Elizabeth I., and Mate Toth. "Animal Models of PTSD: A Critical Review." In Behavioral Neurobiology of PTSD, 47–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/7854_2016_65.
Повний текст джерелаТези доповідей конференцій з теми "PTSD animal model"
Sajja, Sujith V., Matthew P. Galloway, Farhad Ghoddoussi, T. Dhananjeyan, Andrea Kespel, and Pamela VandeVord. "Possible Mechanism of Blast-Induced Neuronal Damage in Hippocampus May Explain Cognitive Deficits." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19545.
Повний текст джерелаЗвіти організацій з теми "PTSD animal model"
Yehuda, Rachel, and Joseph Buxbaum. Molecular Mechanisms Underlying Individual Differences in Response to Stress in a Previously Validated Animal Model of PTSD. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada564271.
Повний текст джерелаYehuda, Rachel, and Joseph Buxbaum. Molecular Mechanisms Underlying Individual Differences in Response to Stress in a Previously Validated Animal Model of PTSD. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada554787.
Повний текст джерелаMorilak, David. Post-Stress Combined Administration of Beta-Receptor and Glucocorticoid Antagonists as a Novel Preventive Treatment in an Animal Model of PTSD. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada538521.
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