ArticleNeurochemical research2014
The unfolded protein response is triggered in rat neurons of the dorsal raphe nucleus after single-prolonged stress.
Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Modulation of the endoplasmic reticulum stress and unfolded protein response mitigates the behavioral effects of early-life stress.Pharmacological reports : PR · 2023Article
- Molecular Mechanisms of IRE1α-ASK1 Pathway Reactions to Unfolded Protein Response in DRN Neurons of Post-Traumatic Stress Disorder Rats.Journal of molecular neuroscience : MN · 2017Article
- Hyperbaric oxygen therapy as a potential treatment for post-traumatic stress disorder associated with traumatic brain injury.Neuropsychiatric disease and treatment · 2016Review
- Single-prolonged stress activates the transcription factor ATF6α branch of the unfolded protein response in rat neurons of dorsal raphe nucleus.Molecular and cellular biochemistry · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dorsal raphe nucleus (DRN) has been suggested playing an important role in the pathophysiology of post-traumatic stress disorder (PTSD), however the underlying cellular mechanisms are not fully understood. The endoplasmic reticulum (ER) is a critical organelle for synthesis of membrane and secretory proteins, and perturbations in ER lead to the unfolded protein response (UPR). In the present experiment, we hypothesized UPR may be associated with the PTSD, and there is an induction of UPR in the DRN neurons of the PTSD-like rats. We first observed the morphological changes of ER in the DRN neurons of the rats exposed to single-prolonged stress (SPS), a model of PTSD, and then we also detected the expression of ER chaperones glucose regulated protein 78 (GRP78) and glucose regulated protein (GRP94) which are two key sensors and mediators of the UPR and are considered an ER stress-specific inducible proteins using methods of western blot and immunohistochemical analysis. Our results demonstrated there were abnormal expansion of ER and up-regulation expression of GRP78 and GRP94 after SPS, which indicated that the UPR was triggered in the DRN neurons of the PTSD-like rats. These results are consistent with our speculation that UPR may be associated with the PTSD, and suggest us the UPR may be a new critical cellular mechanisms of PTSD.
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