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Published on: June 29, 2015
FGF2 blocks PTSD symptoms via an astrocyte-based mechanism
Liang Xia1, Mingzhu Zhai, Liying Wang
1Department of Psychology, School of Aerospace Medicine, The Fourth Military Medical University, No. 169 West Chang'le Road, Xi'an 710032, Shanxi Province, PR China; Department of Neurology, No. 422 Hospital of PLA, No. 3 Hai Bing Road, Zhanjiang 524000, Guangdong Province, PR China.
Abstract:
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.
