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Dergiler / Marmara Medical Journal / 2016 / Cilt: 29 - Sayı: 2

The role of GluN1 activated nitric oxide synthase in a rat model of post-traumatic stress disorder

Beycan Gözde AYHAN
Aslı AYKAÇ
Kutlay GÜR
Banu AYDIN
Ece SEÇGİN
İrem SEVEN
Hülya CABADAK
M Zafer GÖREN
Sayfa
67–72
Yayın Tarihi
2016-04-01
DOI
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors.Keywords: Predator scent

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Amaç & Hipotez:Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD).Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze.
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Temel Bulgular & Veri:An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to detect calmodulin, NOS and GluN1 by immunoblotting.Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05).
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Sonuç & Katkı:The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors.Keywords: Predator scent
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Saldırgan hayvan kokusu testi · nNOS

Özet

Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD).Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to detect calmodulin, NOS and GluN1 by immunoblotting.Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05).Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors.Keywords: Predator scent

Abstract

Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD).Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to detect calmodulin, NOS and GluN1 by immunoblotting.Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05).Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors.Keywords: Predator scent

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Bu Makaleye Atıf Yap

AYHAN, B. G., AYKAÇ, A., GÜR, K., AYDIN, B., SEÇGİN, E., SEVEN, İ., CABADAK, H., GÖREN, M. Z. (2016). The role of GluN1 activated nitric oxide synthase in a rat model of post-traumatic stress disorder. Marmara Medical Journal, Cilt: 29 - Sayı: 2, 67–72. https://ajindex.com/articles/688342

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Kaynakça (2)

  1. Yehuda R. Risk and resilience in posttraumatic stress disorder. J Clinic Psychiatr 2004;65:26-36.
  2. Griffin GD, Charron D, Al-Daccak R. Post-traumatic stress disorder: revisiting adrenergics, glucocorticoids, immune system effects and homeostasis. Clin Transl Immunology 2014;3:e27. doi: 10.1038/cti.2014.26 Zoladz PR, Diamond DM. Current status on behavioral and biological markers of PTSD: a search for clarity in a conflicting literature Neurosci Biobehav Rev 2013;27:860-95. doi: 10.1016/j.neubiorev.2013.03.024 Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52:1048-60. doi:10.1001/archpsyc.1995.03950240066012. Nemeroff CB, Bremner JD, Foa EB, Mayberg HS, North CS, Stein MB. Posttraumatic stress disorder: a state-of-thescience review. J Psychiatr Res 2005;40:1-21. doi: 10.1016/j.jpsychires.2005.07.005 Yehuda R, LeDoux J. Response variation following trauma: a translational neuroscience approach to understanding PTSD. Neuron 207;56: 19-32. doi:10.1016/j.neuron.2007.09.006 Andero R, Ressler KJ. Fear extinction and BDNF: translating animal models of PTSD to the clinic. Genes Brain Behav 2012;11:503-12. doi: 10.1111/j.1601-183X.2012.00801.x Cohen, H., Zohar, J. An animal model of posttraumatic stress disorder: the use of cut-off behavioral criteria. Ann N Y Acad Sci 2004;1032:167-78. doi: 10.1196/annals.1314.014 Adamec R, Muir C, Grimes M, Pearcey K. Involvement of noradrenergic and corticoid receptors in the consolidation of the lasting anxiogenic effects of predator stress. Behav Brain Res 2007;179: 192-207. doi:10.1016/j.bbr.2007.02.001 Cohen H, Kaplan Z, Matar MA, Loewenthal U, Zohar J, Richter-Levin G. Long-lasting behavioral effects of juvenile trauma in an animal model of PTSD associated with a failure of the autonomic nervous system to recover. Eur Neuropsychopharmacol 2006;17:464-77. doi:10.1016/j.euroneuro.2006.11.003 Rauch SL, Shin LM, Phelps EA. Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research – past, present, and future. Biological Psychiatry 2006;60:376–82. doi:10.1016/j.biopsych.2006.06.004 Shin LM, Rauch SL, Pitman RK. Amygdala, medial prefrontal cortex, and hippocampal function in PTSD. Ann NY Acad Sci 2006;1071:67-79. doi: 10.1196/annals.1364.007 Bredt DS. Endogenous nitric oxide synthesis: biological functions and pathophysiology, Free Radic Res 1999;31 577–96. doi:10.1080/10715769900301161 Zhou L, Z