FGF2 blocks PTSD symptoms via an astrocyte-based mechanism
FGF2 blocks PTSD symptoms via an astrocyte-based mechanism
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FGF2 通过基于星形胶质细胞的机制阻断 PTSD 症状
DOI：
10.1016/j.bbr.2013.08.048
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发表时间：
2013-11
影响因子：
2.7
通讯作者：
Wang, Wen
中科院分区：
文献类型：
--
作者：
Xia, Liang;Zhai, Mingzhu;Wang, Liying;Miao, Danmin;Zhu, Xia;Wang, Wen
虽然创伤后应激障碍（PTSD）的特征是创伤性记忆或经历以及唤醒增加，这可以通过抗抑郁药部分缓解，但其潜在的细胞机制尚未完全了解。由于新兴的研究集中在星形胶质细胞在病理性情绪障碍中的关键作用，我们假设存在几种“星形胶质细胞相关”的PTSD机制。本研究采用单次延长应激（SPS）大鼠模型，观察了腹腔注射FGF 2对SPS诱导的PTSD大鼠行为反应的影响，以及对SPS大鼠星形胶质细胞激活的影响。行为学数据显示，腹腔内FGF 2抑制SPS诱导的过度觉醒和焦虑行为;然而，免疫组织化学显示，SPS诱导的星形胶质细胞抑制被腹腔内FGF 2激活。定量Western印迹显示，腹腔内FGF 2上调胶质细胞酸性蛋白（GFAP），但不是NeuN，在海马中的表达。我们认为腹腔注射FGF 2可以通过星形胶质细胞而不是神经元的机制阻断创伤后应激障碍中SPS诱导的恐惧反应和焦虑行为。
Although posttraumatic stress disorder (PTSD) is characterized by traumatic memories or experiences and increased arousal, which can be partly alleviated by antidepressants, the underlying cellular mechanisms are not fully understood. As emerging studies have focused on the critical role of astrocytes in pathological mood disorders, we hypothesized that several ‘astrocyte-related’ mechanisms underlying PTSD exist. In the present study, using the single prolonged stress (SPS) model, we investigated the effects of intraperitoneal FGF2 on SPS-induced PTSD behavior response as well as the astrocytic activation after FGF2 administration in SPS rats. Behavioral data showed that intraperitoneal FGF2 inhibited SPS-induced hyperarousal and anxiety behavior; however, immunohistochemistry showed that SPS-induced astrocytic inhibition was activated by intraperitoneal FGF2. Quantitative western blotting showed that intraperitoneal FGF2 up-regulated glial fibrillary acidic protein (GFAP), but not NeuN, expression in the hippocampus. We suggest that intraperitoneal FGF2 could block the SPS-induced fear response and anxiety behavior in PTSD via astrocyte-based but not neuron-based mechanisms.
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影响因子：
6.2
作者：
N. Belluardo;G. Mudó;X.H. Jiang;D. Condorelli
通讯作者：
N. Belluardo;G. Mudó;X.H. Jiang;D. Condorelli
影响因子：
2.9
作者：
M. Lyons;Robert E. Anderson;F. Meyer
通讯作者：
M. Lyons;Robert E. Anderson;F. Meyer
影响因子：
3.5
作者：
Y. Yamanaka;A. Kitano;K. Takao;A. Prasansuklab;T. Mushiroda;K. Yamazaki;T. Kumada;Minoru Shibata;Yuki Takaoka;T. Awaya;Takeo Kato;T. Abe;N. Iwata;T. Miyakawa;Yusuke Nakamura;T. Nakahata;T. Heike
通讯作者：
Y. Yamanaka;A. Kitano;K. Takao;A. Prasansuklab;T. Mushiroda;K. Yamazaki;T. Kumada;Minoru Shibata;Yuki Takaoka;T. Awaya;Takeo Kato;T. Abe;N. Iwata;T. Miyakawa;Yusuke Nakamura;T. Nakahata;T. Heike
影响因子：
1.9
作者：
P. Cuevas;A. Fernández-Ayerdi;F. Carceller;S. Colin;F. Mascarelli;I. Muñoz-Willery;G. Giménez-Gallego
通讯作者：
P. Cuevas;A. Fernández-Ayerdi;F. Carceller;S. Colin;F. Mascarelli;I. Muñoz-Willery;G. Giménez-Gallego
DOI：
10.1001/jama.2010.1739
发表时间：
2010-12
期刊：
JAMA
影响因子：
--
作者：
R. Pitman
通讯作者：
R. Pitman