ArticleAnalytical cellular pathology (Amsterdam)2021
Mechanism of Chronic Stress-Induced Glutamatergic Neuronal Damage in the Basolateral Amygdaloid Nucleus.
Article in Analytical cellular pathology (Amsterdam), 2021. 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, 16 citations in OpenAlex.
- Sequential decreases in basolateral amygdala response to threat predict failure to recover from PTSD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- From trauma to depression: structural, synaptic, epigenetic, and molecular pathways linking early stress to lifelong vulnerability.Frontiers in psychiatry · 2025Review
- Norepinephrine-Activated p38 MAPK Pathway Mediates Stress-Induced Cytotoxic Edema of Basolateral Amygdala Astrocytes.Brain sciences · 2024Article
- The effects of prolonged stress exposure on the brain of rats and insights to understand the impact of work-related stress on caregivers.Frontiers in behavioral neuroscience · 2023Article
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8 authors at 1 institution in 1 country.
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Abstract
Stress is a ubiquitous part of our life, while appropriate stress levels can help improve the body's adaptability to the environment. However, sustained and excessive levels of stress can lead to the occurrence of multiple devastating diseases. As an emotional center, the amygdala plays a key role in the regulation of stress-induced psycho-behavioral disorders. The structural changes in the amygdala have been shown to affect its functional characteristics. The amygdala-related neurotransmitter imbalance is closely related to psychobehavioral abnormalities. However, the mechanism of structural and functional changes of glutamatergic neurons in the amygdala induced by stress has not been fully elucidated. Here, we identified that chronic stress could lead to the degeneration and death of glutamatergic neurons in the lateral amygdaloid nucleus, resulting in neuroendocrine and psychobehavioral disorders. Therefore, our studies further suggest that the Protein Kinase R-like ER Kinase (PERK) pathway may be therapeutically targeted as one of the key mechanisms of stress-induced glutamatergic neuronal degeneration and death in the amygdala.
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