Single prolonged stress increases contextual freezing and the expression of glycine transporter 1 and vesicle-associated membrane protein 2 mRNA in the hippocampus of rats

Iwamoto, Yasuyuki; Morinobu, Shigeru; Takahashi, Terumichi; Yamawaki, Shigeto

doi:10.1016/j.pnpbp.2006.12.010

Cited by 93 publications

(65 citation statements)

References 36 publications

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“…For example, in this model the hypothalamus-pituitary-adrenal axis provides rapid negative feedback after administration of glucocorticoid [14] to increase anxiety behavior in the elevated plus maze [15], increase contextual freezing [16], and produces an exaggerated acoustic startle response (ASR) [17]. These changes support the validity of SPS as an animal model of PTSD.…”

Section: Introductionmentioning

confidence: 64%

“…EPM was used to determine the behavior of approach-avoidance conflict in rats [16]. The apparatus consisted of two opposing arms (50 cm×10 cm) enclosed by 40 cm high side and end walls (closed arms), the other two arms were not installed with walls (open arms) with the entire maze (DigBehav, Jiliang Co. Ltd., Shanghai, China) elevated 50 cm above the floor.…”

Section: Elevated Plus Maze Test (Epmt)mentioning

confidence: 99%

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Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

et al. 2017

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Section: Introductionmentioning

confidence: 64%

Section: Elevated Plus Maze Test (Epmt)mentioning

confidence: 99%

Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

et al. 2017

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“…Çeşitli kanıtlar ile zarar veren (nocuous) stres modülasyonlarında dorsal rafe çekirdeğinin ana bileşen olarak rol oynadığı ortaya çık-mıştır. Çalışmalarda tek uzatılmış stres (single prolonged stress-SPS) oluşturulmuş sıçanların TSSB bozukluğu ile ilişkili semptomları taklit eden davranışsal anormallikler sergiledikleri vurgulanmıştır (36)(37)(38) Mitokondriyal işlev bozuklukları strese bağlı ruhsal bozukluklarda anahtar bileşen olarak kabul edilir. Beyinde oluşan yapısal ve fonksiyonel değişim olasıkları arasında tekrarlayan ya da kronik strese tepkilerin mitokondri merkezli olabileceğine dair kanıtlar giderek güçlenmektedir (43,44).…”

Section: Travma Sonrası Stres Bozukluğu Ve Apoptozunclassified

Post-Traumatic Stress Disorder: The Importance of Apoptosis

Aykaç¹,

Cabadak²

2016

Clin Exp Health Sci

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Öz AbstractApoptosis is programmed cell death, which actively occurs in many physiological processes. It can be triggered in two ways: (i) defects in growth factor, DNA damage, and other many factors that can cause cellular stress, which is an intracellular pathway, and (ii) ligand binding to death receptors and activation of caspases. The apoptotic cell count can be determined by the health of the whole organism. A higher apoptotic ratio can indicate a decrease in the number of cells and tissue damage, while a lower apoptotic ratio can indicate an increase in the number of cells. Irregularity in apoptotic signals can play primary or secondary roles in various diseases/disorders. Research on apoptosis depends on neurodegeneration has been initiated in the past few years. Definition of apoptotic signal pathways and apoptotic regulation and determination of pro-and anti-apoptotic genes are the main topics that have accelerated research on apoptosis. Neurodegenerative disorders such as post-traumatic stress disorder neuronal damage associated with changes in brain structure and function may be related to the mitochondrial stresses. In physiological conditions, apoptosis is crucial for the organism, while in pathological conditions, apoptosis can cause uncontrolled cell division. Development of therapeutic medicine that inhibits the cell death may be the new choice of treatment for neurodegenerative diseases/disorders. Keywords: Stress, mitochondria, B-cell lymphoma -2 (Bcl-2), cell death GİRİŞHücre ölümü mekanik hasar, oksijen yokluğu ve toksik maddelerin etkisi ile gerçekleşen hasar yolu (nekrotik); programlanmış hücre ölümü (apoptotik); veya uzun ömürlü proteinlerin, organellerin ve sitoplazmik parçacıkların parçalanmasıyla gerçekleşen otofaji yolu ile ölüm olmak üzere üç tipte gerçekleşmektedir. Nekroz her zaman patolojik durumlarda ortaya çıkarken, apoptoz fizyolojik veya bazen patolojik koşullarda ortaya çıkan ölüm şeklidir. Nekroz durumunda hücre boyutunda artış, hücre organellerinin su alarak şişmesi, hücre zarında parçalanmalar gö-rülür. Apoptoz durumunda ise hücrede küçülme, sitoplazma yoğunluğunda artış, hücrenin büzülmesi ve kıvrımlı görüntü oluşturması gözle-nir. Nekroz sonucu hücre içi maddelerin dağılmasıyla inflamasyon oluşurken, apoptoz sonucunda hücre inflamasyona uğramadan ortamdan temizlenmektedir. Nekrozdan farklı olarak apoptoz aktif, metabolik, genetik olarak kodlanmış ve evrimsel olarak seçilen ölüm yoludur.Hücrede apoptozun indüklenmesine aracılık eden pek çok mekanizma vardır. Hücrenin duyarlılığı pro-ya da anti-apoptotik proteinlerin ekspresyonu gibi birçok faktöre bağlı olarak değişebilir. Apoptotik sinyallemede düzensizlik çeşitli hastalıklarda primer ya da sekonder rol oynamaktadır. Yetersiz apoptozun neden olduğu hastalıklar arasında kanser, otoimmünite, kronik enfeksiyonlar, iskemi-reperfüzyon, Ailesel Akdeniz Ateşi, tip 2 Diabetes Mellitus ve nörodejeneratif hastalıkları saymak mümkündür (1-4).Biliş ve duygu durumun düzenlenmesinden sorumlu hipokampus ve hipokampus ile bağlantısı ola...

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“…Diagnostic symptoms for PTSD include re-experiencing the original trauma through flashbacks or nightmares, avoidance of stimuli associated with the trauma and increased arousal. Single-prolonged stress (SPS), an animal model of PTSD, has been extensively developed and employed in the investigation of PTSD (1)(2)(3). The three areas of the brain whose function may be altered in PTSD have been identified as the prefrontal cortex, the amygdala and the hippocampus, among which, the hippocampus is a key organ of the limbic system involved in learning and memory, as well as being a regulatory center for the stress response (4).…”

Section: Introductionmentioning

confidence: 99%

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

Tong

Peng

et al. 2014

Molecular Medicine Reports

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Abstract. Vitamin D signaling not only controls calcium (Ca 2+ ) and phosphorus uptake and transport, but also correlates with neurocognitive decline and neurodegenerative diseases. Almost all actions of Vitamin D are mediated by the transcription factor, vitamin D receptor (VDR), which has been widely identified in the central nervous system. Although previous studies have substantially advanced the understanding of the action of VDR in the brain, much remains unknown concerning how VDR relates to stress. Multiple lines of evidence indicate that the downregulation of L-type voltage-sensitive Ca 2+ -channels α-1C (LVSCC-A1C) by vitamin D in hippocampal neurons is able to reduce the influx and excitotoxic effects of Ca 2+ to neurons. Along these lines, the purpose of the present study was to analyze the relative expression of VDR in the hippocampus of rats exposed to single prolonged stress (SPS) as a putative animal model for human post-traumatic stress disorder (PTSD). Furthermore, changes in the levels of expression of LVSCC-A1C and Ca 2+ (neurotransmitter content) were examined during the onset periods of PTSD. The results revealed an increase in the expression of VDR at 1, 3 and 7 days post-stress compared with the control group. The intracellular free Ca 2+ levels in the hippocampus increased 1 day after SPS exposure, and then decreased gradually to the normal level at 14 days, consistent with the expression pattern of LVSCC-A1C. These results indicated that VDR may be involved in the pathogenesis of SPS rats, thereby providing an alternative preparation to search for optimal therapeutic strategies for PTSD. IntroductionPost-traumatic stress disorder (PTSD) is a severe anxiety disorder that may develop following exposure to any threat or injury that results in psychological trauma. Diagnostic symptoms for PTSD include re-experiencing the original trauma through flashbacks or nightmares, avoidance of stimuli associated with the trauma and increased arousal. Single-prolonged stress (SPS), an animal model of PTSD, has been extensively developed and employed in the investigation of PTSD (1-3). The three areas of the brain whose function may be altered in PTSD have been identified as the prefrontal cortex, the amygdala and the hippocampus, among which, the hippocampus is a key organ of the limbic system involved in learning and memory, as well as being a regulatory center for the stress response (4).Alterations in brain neurochemistry have been linked with neuropsychiatric disorders, including schizophrenia, Alzheimer's disease, depression and cognitive decline. Previous studies have identified a positive association between vitamin D signaling and cognitive function (5). Vitamin D may regulate neurotransmission, neuroprotection and neuroimmunomodulation as a neurosteroid hormone (5,6), in addition to its critical role in calcium (Ca 2+ ) and phosphorous regulation and skeletal mineralization (7). Hypovitaminosis D is associated with several neuropsychiatric disorders, including dementia, Parkinson's d...

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Single prolonged stress increases contextual freezing and the expression of glycine transporter 1 and vesicle-associated membrane protein 2 mRNA in the hippocampus of rats

Cited by 93 publications

References 36 publications

Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

Post-Traumatic Stress Disorder: The Importance of Apoptosis

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

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