What Happened in the Hippocampal Axon in a Rat Model of Posttraumatic Stress Disorder
- PDF / 7,985,240 Bytes
- 15 Pages / 595.276 x 790.866 pts Page_size
- 21 Downloads / 166 Views
ORIGINAL RESEARCH
What Happened in the Hippocampal Axon in a Rat Model of Posttraumatic Stress Disorder Yadi Guan1,2 · Xinzhao Chen1 · Beiying Zhao1 · Yuxiu Shi1 · Fang Han1 Received: 21 May 2020 / Accepted: 3 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Studies from postmortem and animal models have revealed altered synapse morphology and function in the brain of posttraumatic stress disorder (PTSD). And the effects of PTSD on dendrites and spines have been reported, however, the effection on axon include microtubule (MT) and synaptic vesicles of presynaptic elements remains unknown. Hippocampus is involved in abnormal memory in PTSD. In the present study, we used the single prolonged stress (SPS) model to mimic PTSD. Quantitative real-time polymerase chain reaction (RT-qPCR) and high-throughput sequencing (GSE153081) were utilized to analyze differentially expressed genes (DEGs) in the hippocampus of control and SPS rats. Immunofluorescence and western blotting were performed to examine change in axon-related proteins. Synaptic function was evaluated by measuring miniature excitatory postsynaptic currents (mEPSCs). RNA-sequencing analysis revealed 230 significantly DEGs between the control and SPS groups. Gene Ontology analysis revealed upregulation in axonemal assembly, MT formation, or movement, but downregulation in axon initial segment and synaptic vesicles fusion in the hippocampus of SPS rats. Increased expression in tau, β-tubulin MAP1B, KIF9, CCDC40, DNAH12 and decreased expression in p-tau, stathmin suggested SPS induced axon extension. Increased protein expression in VAMP, STX1A, Munc18-1 and decreased expression in synaptotagmin-1 suggested SPS induced more SNARE complex formation but decreased ability in synaptic vesicle fusion to presynaptic active zone membrane in the hippocampus of SPS rats. Further, low mEPSC frequency in SPS rats indicated dysfunction in presynaptic membrane. These results suggest that axon extension and synaptic vesicles fusion abnormality are involved in dysfunction of PTSD. Keywords Microtubules · Axon · Presynaptic · Single prolonged stress · Posttraumatic stress disorder Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10571-020-00960-w) contains supplementary material, which is available to authorized users. * Fang Han [email protected] Yadi Guan [email protected] Xinzhao Chen [email protected] Beiying Zhao [email protected] Yuxiu Shi [email protected] 1
PTSD Laboratory, Department of Histology and Embryology, Basic Medical University, China Medical University, Shenyang 110122, China
Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang 110022, Liaoning Province, China
2
Introduction Posttraumatic stress disorder (PTSD) is a persistent, serious mental disorder brought about by traumatic events such as natural disasters, traffic accidents, criminal violence, and abuse (Heneka et al. 2018). The diagnostic symptoms include intrusio
Data Loading...
