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Dynamic Expression of Glutamate Receptor of Hippocampus, Prefrontal Cortex and Amygdala in an Animal Model of PTSD

Author: SongZuoLin
Tutor: LuoJianHong
School: Zhejiang University
Course: Neurobiology
Keywords: Post-traumatic stress disorder Hippocampal Prefrontal cortex Amygdala NR1 GluR1
CLC: R749.5
Type: Master's thesis
Year: 2007
Downloads: 153
Quote: 1
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Abstract


Post-traumatic stress disorder (Post-traumatie stress disorder, PTSD) refers to react violently threatening, catastrophic events experienced or witnessed extraordinary. Understanding of post-traumatic stress disorder than 100 years of history, has been the title of \The first time in the U.S. mental disorders in the third edition of the Diagnostic and Statistical Manual (DSM-Ⅲ) definition of PTSD, and describe the re-experience the trauma, avoidance, hypervigilance three main symptoms. Re-experience the trauma symptoms include nightmare flashback memories, traumatic flashbacks; The avoidance symptoms including deliberately forgotten, do not want to talk about or retrospect; hypervigilance symptoms include severe panic reactions, sleep disorders, attention difficulty concentrating. Study PTSD is the most functional brain imaging techniques, mainly PET and fMRI. Some studies suggest that smaller hippocampal volume in PTSD patients, and a positive correlation with the severity of PTSD symptoms; while others think that the the PTSD patients hippocampus volume does not change. Some studies found that PTSD patients with advanced left amygdala activity increased in smaller but reduce early right amygdala response. PTSD patients with prefrontal volume seems to be smaller, low response in the trial of cognitive tasks. Glutamate receptor family is divided into two major categories of ionotropic glutamate receptors and metabotropic glutamate receptors. Ionotropic glutamate receptor selective agonists can be divided into the NMDA receptor, AMPA receptors and KA receptors. Ionotropic glutamate receptor-mediated excitatory synaptic transmission in the central nervous system. NMDA receptors are composed by NR1, NR2 or NR3 subunit heteromeric molecules. Known NR1 subunit is an essential component of the NMDA receptor in different NR2 subunits NR1 assembly formed having different channel characteristics of the NMDA receptor subtype. NMDA receptors are ligand-gated ion channels in a voltage-dependent channel opening requires not only glutamate and glycine are working together, need to lift Mg 2 channel blockers. AMPA receptors are mainly by the GluR1, GluR2, GluR3 and GluR4 four kinds of subunit composition, now that AMPA receptors are composed of four subunit tetramer, both may be formed the same dimer may also be formed heteropolymer. AMPA receptor-mediated fast excitatory synaptic transmission in the central nervous system. AMPA receptor activation caused by cell membrane partially depolarized, lift Mg 2 blockade of the NMDA receptor channel when the depolarization reaches a certain level. Studies have shown that activation of the NMDA receptor channel helps AMPA receptors inserted into the membrane surface of dendritic spines, synaptic transmission performance significantly enhanced. There is no cure for the treatment of PTSD, is limited to the replacement therapy with other mental diseases. Previous pharmacological studies have shown that blocking AMPA receptors can alleviate the symptoms of PTSD, but specifically which one or which in several brain areas involved, and the possible molecular mechanism is unclear. Functional imaging study, PTSD patients may exist amygdala, hippocampus, prefrontal cortex structure and function of several brain areas changes. Known glutamate receptor plays an important role in synaptic plasticity and learning and memory, and is closely related to PTSD and fear memory. Therefore, in this study, we study a rat model of PTSD glutamate receptor expression changes in the three brain regions of the hippocampus, the prefrontal cortex, amygdala, to explore the molecular mechanisms of of PTSD sensitization symptoms for the clinical treatment of PTSD provide some theoretical basis. Until now, not yet able to fully simulate human disease animal models of PTSD, can only simulate some symptoms of PTSD. Rau V, DeCola JP study, we established a rat model of PTSD (the model can effectively simulate the PTSD one important feature - sensitization); rats were sacrificed, the brain was immediately isolated on ice hippocampus, forehead cortex, amygdala; reaction for detection of NR1, GluR1 content according to the classic method of extracting brain tissue and membrane proteins; immunoblotting. We found that: (1) in the hippocampus of PTSD group membrane protein GluR1 content significantly increased and maintained at a high level. Suggesting that PTSD may affect the the hippocampal synaptic structure and function, leading to behavioral sensitization. (2) the first frontal skin of PTSD group and Control group neuron cell membrane surface AMPA receptors and NMDA receptor content was significantly lower than the Naive group, the results suggest that stress may cause prefrontal cortex activity reduce, and Imageology The results are consistent. (3) in the amygdala, PTSD group NR1 content than the Control group increased NR1 an increase in the total protein of PTSD group may be related to fear memory related.

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