The Role of Glucocorticoid Receptor in Brain Stress Response
Author Information
Author(s): Adzic Miroslav, Djordjevic Ana, Demonacos Constantinos, Krstic-Demonacos Marija, Radojcic Marija B.
Primary Institution: VINCA Institute of Nuclear Sciences
Hypothesis
Mitochondrial glucocorticoid receptor and its phosphoisoforms may affect mitochondrial functions in a stress-dependent manner.
Conclusion
Chronic stress leads to increased mitochondrial glucocorticoid receptor levels, which are primarily phosphorylated at serine 232, affecting mitochondrial gene expression and pro-apoptotic signaling.
Supporting Evidence
- Chronic stress increased mitochondrial glucocorticoid receptor levels in both hippocampus and prefrontal cortex.
- Phosphorylation at serine 232 was predominant under chronic stress conditions.
- Expression of mitochondrial COX 1 and COX 3 genes was differentially regulated by stress in the two brain regions.
Takeaway
When rats are stressed, their brain cells change how they use energy and can become more likely to die. This study looks at how a specific protein in the brain helps with this process.
Methodology
The study involved Wistar male rats subjected to different stress models, followed by analysis of mitochondrial glucocorticoid receptor levels and gene expression using Western blot and RT-qPCR.
Potential Biases
Potential bias in the interpretation of stress effects due to the specific animal model used.
Limitations
The study was limited to male Wistar rats, which may not represent other populations or species.
Participant Demographics
Adult (3 months old) Wistar male rats, body mass 330–400 g.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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