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Exploring Molecular Changes in the Extended Amygdala Induced by Chronic Corticosterone Administration

Summary

Researchers studied how prolonged stress hormone exposure affects the brain’s emotional center in mice. They found that chronic corticosterone treatment caused depression-like behaviors and specific molecular changes in different parts of the amygdala, a brain region crucial for processing emotions. These findings help explain how chronic stress disrupts the brain’s normal stress-regulation system and contributes to depression and other psychiatric conditions.

Background

Chronic stress is a significant risk factor for psychiatric disorders including depression. The hypothalamic-pituitary-adrenal (HPA) axis normally regulates stress responses through glucocorticoid release, but severe chronic stress can disrupt this system and contribute to psychiatric disorders. However, the molecular-level brain changes resulting from HPA axis dysfunction remain unclear.

Objective

The study aimed to investigate molecular changes in the extended amygdala following chronic corticosterone administration as a model of chronic stress-induced HPA axis dysfunction. The researchers sought to identify subnuclei-specific molecular alterations in this emotionally-relevant brain region.

Results

Chronically-treated mice exhibited depression-like symptoms including body weight loss, decreased activity, anhedonia, and increased despair behavior. RNA-seq analysis revealed that different molecular changes were observed in specific subnuclei of the extended amygdala in response to chronic corticosterone administration.

Conclusion

The study demonstrates that chronic corticosterone administration induces distinct molecular changes across different subnuclei of the extended amygdala, contributing to understanding of neural circuit alterations induced by chronic stress and potentially underlying psychiatric symptoms.
  • Published in:International Journal of Neuropsychopharmacology,
  • Study Type:Experimental Animal Study,
  • Source: 10.1093/ijnp/pyae059.586, PMID: PMC11814659
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