A Recent VA Rules Change and the Traumatic Event Requirement in PTSD
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 12/2010; 304(21):2409-10. DOI: 10.1001/jama.2010.1739
- [Show abstract] [Hide abstract]
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.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.