Research reportFGF2 blocks PTSD symptoms via an astrocyte-based mechanism

- Intraperitoneal administration of FGF2 decreased the freezing time and anxiety behavior in rats.
- Single prolonged stress (SPS) induced astrocytic inhibition in the hippocampus.
- Astrocytic inhibition may be reversed by FGF2 application.
- SPS and FGF2 application had no effect on neurons.
- FGF2 blocks the PTSD symptoms via the astrocyte-based mechanism but not neurons.

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.