NDLI: Increased Neuronal Apoptosis in Medial Prefrontal Cortex is Accompanied with Changes of Bcl-2 and Bax in a Rat Model of Post-Traumatic Stress Disorder

Content Provider	Springer Nature Link
Author	Li, Yana Han, Fang Shi, Yuxiu
Copyright Year	2013
Abstract	Post-traumatic stress disorder (PTSD) is an anxiety disorder caused by traumatic experience, which affects a patient’s quality of life and social stability. The objective of this study was to determine the apoptosis-related genes B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) expressions and medial prefrontal cortex (mPFC) neuronal apoptosis after PTSD in rat model and therefore to provide experimental evidence to reveal PTSD pathogenesis. The single-prolonged stress (SPS) method was used to set up the rat PTSD models. Chemiluminescence was used to determine serum corticosterone levels. Neuronal apoptosis was detected using transmission electron microscopy, Hoechst staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Immunohistochemistry, immunofluorescence, RT-PCR, and Western blot were used to detect the expressions of Bcl-2 and Bax protein in mPFC. Our results showed an increased mPFC neuronal apoptosis after SPS stimulation. The number of apoptotic cells peaked on day 7. The expressions of Bcl-2 and Bax peaked on days 4 and 7. The Bcl-2/Bax ratio elevated on days 1 and 4 but decreased markedly on day 7. These results indicated that SPS stimulation increased the number of apoptotic neurons, up-regulated the expressions of Bcl-2 and Bax, and altered the Bcl-2/Bax ratio in the mPFC of PTSD rats.
Starting Page	127
Ending Page	137
Page Count	11
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	51
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2013-02-05
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Post-traumatic stress disorder Medial prefrontal cortex Bcl-2 Bax Neuronal apoptosis Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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