scholarly journals Ca v 1.2 channels mediate persistent chronic stress-induced behavioral deficits that are associated with prefrontal cortex activation of the p25/Cdk5-glucocorticoid receptor pathway

2017 ◽  
Vol 7 ◽  
pp. 27-37 ◽  
Author(s):  
Charlotte C. Bavley ◽  
Delaney K. Fischer ◽  
Bryant K. Rizzo ◽  
Anjali M. Rajadhyaksha
Keyword(s):  
Prefrontal Cortex ◽  
Glucocorticoid Receptor ◽  
Chronic Stress ◽  
Behavioral Deficits

scholarly journals Chronic Stress Alters Astrocyte Morphology in Mouse Prefrontal Cortex

2021 ◽  
Author(s):  
Sierra A. Codeluppi ◽  
Dipashree Chatterjee ◽  
Thomas D. Prevot ◽  
Keith A. Misquitta ◽  
Etienne Sibille ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Fluorescent Protein ◽  
Glial Fibrillary Acid Protein ◽  
Behavioral Deficits ◽  
Sholl Analysis ◽  
Acid Protein ◽  
Potential Link ◽  
Green Fluorescent ◽  
Stress Models

AbstractBackgroundNeuromorphological changes are consistently reported in the prefrontal cortex (PFC) of patients with stress-related disorders and in rodent stress models, but the effects of stress on astrocyte morphology and potential link to behavioral deficits are relatively unknown.MethodsTo answer these questions, transgenic mice expressing green fluorescent protein (GFP) under the glial fibrillary acid protein (GFAP) promotor were subjected to 7, 21 or 35 days of chronic restraint stress (CRS). CRS behavioral effects on anhedonia- and anxiety-like behaviours were measured using the sucrose intake and the PhenoTyper tests, respectively. PFC GFP+ or GFAP+ cells morphology was assessed using Sholl analysis and associations with behavior were determined using correlation analysis.ResultsCRS-exposed mice displayed anxiety-like behavior at 7, 21 and 35 days and anhedonia-like behavior at 35 days. Analysis of GFAP+ cell morphology revealed significant atrophy of distal processes following 21 and 35 days of CRS. CRS induced similar decreases in intersections at distal radii for GFP+ cells, accompanied by increased proximal processes. Additionally, the number of intersections at the most distal radius step significantly correlated with time spent in the shelter zone in the PhenoTyper test (r=-0.581, p<0.01) for GFP+ cells and with behavioural emotionality calculated by z-scoring all behavioral measured deficits, for both GFAP+ and GFP+ cells (r=-0.400, p<0.05; r=-0.399, p<0.05).ConclusionChronic stress exposure induces a progressive atrophy of cortical astroglial cells, potentially contributing to maladaptive neuroplastic changes associated with stress-related disorders.

scholarly journals Chronic Stress Alters Astrocyte Morphology in Mouse Prefrontal Cortex

2021 ◽  
Author(s):  
Sierra A Codeluppi ◽  
Dipashree Chatterjee ◽  
Thomas D Prevot ◽  
Yashika Bansal ◽  
Keith A Misquitta ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Fluorescent Protein ◽  
Behavioral Changes ◽  
Glial Fibrillary Acid Protein ◽  
Behavioral Deficits ◽  
Acid Protein ◽  
Potential Link ◽  
Green Fluorescent ◽  
Stress Models

Abstract Background Neuromorphological changes are consistently reported in the prefrontal cortex (PFC) of patients with stress-related disorders and in rodent stress models, but the effects of stress on astrocyte morphology and potential link to behavioral deficits are relatively unknown. Methods To answer these questions, transgenic mice expressing green fluorescent protein (GFP) under the glial fibrillary acid protein (GFAP) promotor were subjected to 7, 21 or 35 days of chronic restraint stress (CRS). CRS induced behavioral effects on anhedonia- and anxiety-like behaviors were measured using the sucrose intake and the PhenoTyper tests, respectively. PFC GFP+ or GFAP+ cells morphology was assessed using Sholl analysis and associations with behavior were determined using correlation analysis. Results CRS-exposed male and female mice displayed anxiety-like behavior at 7, 21 and 35 days and anhedonia-like behavior at 35 days. Analysis of GFAP+ cell morphology revealed significant atrophy of distal processes following 21 and 35 days of CRS. CRS induced similar decreases in intersections at distal radii for GFP+ cells, accompanied by increased proximal processes. In males, the number of intersections at the most distal radius step significantly correlated with anhedonia-like behavior (r=0.622, p&lt;0.05) for GFP+ cells and with behavioral emotionality calculated by z-scoring all behavioral measured deficits (r=-0.667, p&lt;0.05). Similar but not significant correlations were observed in females. No correlation between GFP+ cell atrophy with anxiety-like behavior was found. Conclusion Chronic stress exposure induces a progressive atrophy of cortical astroglial cells, potentially contributing to maladaptive neuroplastic and behavioral changes associated with stress-related disorders.

Pituitary glucocorticoid receptor deletion reduces vulnerability to chronic stress

2011 ◽  
Vol 36 (4) ◽  
pp. 579-587 ◽  
Author(s):  
Klaus V. Wagner ◽  
Xiao-Dong Wang ◽  
Claudia Liebl ◽  
Sebastian H. Scharf ◽  
Marianne B. Müller ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Chronic Stress

scholarly journals Chronic Stress Induced Remodeling of the Prefrontal Cortex: Structural Re-Organization of Microglia and the Inhibitory Effect of Minocycline

2012 ◽  
Vol 23 (8) ◽  
pp. 1784-1797 ◽  
Author(s):  
M. Hinwood ◽  
R. J. Tynan ◽  
J. L. Charnley ◽  
S. B. Beynon ◽  
T. A. Day ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Inhibitory Effect

scholarly journals Mitochondrial gene signature in the prefrontal cortex for differential susceptibility to chronic stress

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Meltem Weger ◽  
Daniel Alpern ◽  
Antoine Cherix ◽  
Sriparna Ghosal ◽  
Jocelyn Grosse ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dna ◽  
Prefrontal Cortex ◽  
Mitochondrial Dysfunction ◽  
Chronic Stress ◽  
Mitochondrial Gene ◽  
Brain Regions ◽  
Mitochondrial Gene Expression ◽  
Data Set ◽  
A Genome

Abstract Mitochondrial dysfunction was highlighted as a crucial vulnerability factor for the development of depression. However, systemic studies assessing stress-induced changes in mitochondria-associated genes in brain regions relevant to depression symptomatology remain scarce. Here, we performed a genome-wide transcriptomic study to examine mitochondrial gene expression in the prefrontal cortex (PFC) and nucleus accumbens (NAc) of mice exposed to multimodal chronic restraint stress. We identified mitochondria-associated gene pathways as most prominently affected in the PFC and with lesser significance in the NAc. A more detailed mitochondrial gene expression analysis revealed that in particular mitochondrial DNA-encoded subunits of the oxidative phosphorylation complexes were altered in the PFC. The comparison of our data with a reanalyzed transcriptome data set of chronic variable stress mice and major depression disorder subjects showed that the changes in mitochondrial DNA-encoded genes are a feature generalizing to other chronic stress-protocols as well and might have translational relevance. Finally, we provide evidence for changes in mitochondrial outputs in the PFC following chronic stress that are indicative of mitochondrial dysfunction. Collectively, our work reinforces the idea that changes in mitochondrial gene expression are key players in the prefrontal adaptations observed in individuals with high behavioral susceptibility and resilience to chronic stress.

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