scholarly journals Functional Contribution of the Medial Prefrontal Circuitry in Major Depressive Disorder and Stress-Induced Depressive-Like Behaviors

2021 ◽  
Vol 15 ◽  
Author(s):  
Thibault P. Bittar ◽  
Benoit Labonté
Keyword(s):  
Major Depressive Disorder ◽  
Animal Models ◽  
Depressive Disorder ◽  
Chronic Stress ◽  
Emotional Processing ◽  
Recent Literature ◽  
Behavioral Responses ◽  
Major Depressive ◽  
Males And Females ◽  
Prefrontal Circuitry

Despite decades of research on the neurobiology of major depressive disorder (MDD), the mechanisms underlying its expression remain unknown. The medial prefrontal cortex (mPFC), a hub region involved in emotional processing and stress response elaboration, is highly impacted in MDD patients and animal models of chronic stress. Recent advances showed alterations in the morphology and activity of mPFC neurons along with profound changes in their transcriptional programs. Studies at the circuitry level highlighted the relevance of deciphering the contributions of the distinct prefrontal circuits in the elaboration of adapted and maladapted behavioral responses in the context of chronic stress. Interestingly, MDD presents a sexual dimorphism, a feature recognized in the molecular field but understudied on the circuit level. This review examines the recent literature and summarizes the contribution of the mPFC circuitry in the expression of MDD in males and females along with the morphological and functional alterations that change the activity of these neuronal circuits in human MDD and animal models of depressive-like behaviors.

scholarly journals Brain functional effects of electroconvulsive therapy during emotional processing in major depressive disorder

2020 ◽  
Vol 13 (4) ◽  
pp. 1051-1058
Author(s):  
Verena Enneking ◽  
Fanni Dzvonyar ◽  
Kerstin Dück ◽  
Katharina Dohm ◽  
Dominik Grotegerd ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Electroconvulsive Therapy ◽  
Emotional Processing ◽  
Major Depressive

Shared Transcriptional Signatures in Major Depressive Disorder and Mouse Chronic Stress Models

2020 ◽  
Vol 87 (9) ◽  
pp. S222
Author(s):  
Joseph Scarpa ◽  
Mena Fatma ◽  
Yong-Hwee E. Loh ◽  
Said Romaric Traore ◽  
Théo Stefan ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Chronic Stress ◽  
Major Depressive ◽  
Stress Models

scholarly journals Animal models of major depressive disorder and the implications for drug discovery and development

2019 ◽  
Vol 14 (4) ◽  
pp. 365-378 ◽  
Author(s):  
Konstantin A. Demin ◽  
Maxim Sysoev ◽  
Maria V. Chernysh ◽  
Anna K. Savva ◽  
Mamiko Koshiba ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Drug Discovery ◽  
Animal Models ◽  
Depressive Disorder ◽  
Major Depressive ◽  
Drug Discovery And Development

scholarly journals Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

2017 ◽  
Vol 1 ◽  
pp. 247054701772045 ◽  
Author(s):  
Mounira Banasr ◽  
Ashley Lepack ◽  
Corey Fee ◽  
Vanja Duric ◽  
Jaime Maldonado-Aviles ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Protein Expression ◽  
Neuropeptide Y ◽  
Chronic Stress ◽  
Gabaergic Interneurons ◽  
Chronic Unpredictable Stress ◽  
Major Depressive

Background Evidence continues to build suggesting that the GABAergic neurotransmitter system is altered in brains of patients with major depressive disorder. However, there is little information available related to the extent of these changes or the potential mechanisms associated with these alterations. As stress is a well-established precipitant to depressive episodes, we sought to explore the impact of chronic stress on GABAergic interneurons. Methods Using western blot analyses and quantitative real-time polymerase chain reaction, we assessed the effects of five-weeks of chronic unpredictable stress exposure on the expression of GABA-synthesizing enzymes (GAD65 and GAD67), calcium-binding proteins (calbindin, parvalbumin, and calretinin), and neuropeptides co-expressed in GABAergic neurons (somatostatin, neuropeptide Y, vasoactive intestinal peptide, and cholecystokinin) in the prefrontal cortex and hippocampus of rats. We also investigated the effects of corticosterone and dexamethasone exposure on these markers in vitro in primary cortical and hippocampal cultures. Results We found that chronic unpredictable stress induced significant reductions of GAD67 protein levels in both the prefrontal cortex and hippocampus of chronic unpredictable stress-exposed rats but did not detect changes in GAD65 protein expression. Similar protein expression changes were found in vitro in cortical neurons. In addition, our results provide clear evidence of reduced markers of interneuron population(s), namely somatostatin and neuropeptide Y, in the prefrontal cortex, suggesting these cell types may be selectively vulnerable to chronic stress. Conclusion Together, this work highlights that chronic stress induces regional and cell type-selective effects on GABAergic interneurons in rats. These findings provide additional supporting evidence that stress-induced GABA neuron dysfunction and cell vulnerability play critical roles in the pathophysiology of stress-related illnesses, including major depressive disorder.

scholarly journals Reconsidering Animal Models of Major Depressive Disorder in the Elderly

2016 ◽  
Vol 8 ◽  
Author(s):  
Shigenobu Toda ◽  
Yoshio Iguchi ◽  
Ziqiao Lin ◽  
Hiromi Nishikawa ◽  
Tatsuya Nagasawa ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Animal Models ◽  
Depressive Disorder ◽  
The Elderly ◽  
Major Depressive

scholarly journals Molecular mechanism of reward treatment ameliorating chronic stress-induced depressive-like behavior assessed by sequencing miRNA and mRNA in medial prefrontal cortex

2020 ◽  
Author(s):  
Tingting An ◽  
Zhenhua Song ◽  
Jin-Hui Wang
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Molecular Mechanism ◽  
Chronic Stress ◽  
Medial Prefrontal Cortex ◽  
Differentially Expressed ◽  
Mild Stress ◽  
Major Depressive ◽  
Differentially Expressed Mirnas

Abstract Background Major depressive disorder (MDD) is a disease that seriously endangers human health and mental state. Chronic stress and lack of reward may reduce the function of the brain's reward circuits, leading to major depressive disorder. The effect of reward treatment on chronic stress-induced depression-like behaviors and its molecular mechanism in the brain remain unclear.Methods Mice were divided into the groups of control, chronic unpredictable mild stress (CUMS), and CUMS-companion. Mice of CUMS group was performed by CUMS for 4 weeks, and CUMS-companion group was treated by CUMS accompanied with companion. The tests of sucrose preference, Y-maze, and forced swimming were conducted to assess depression-like behaviors or resilience. High-throughput sequencing was used to analyze mRNA and miRNA profiles in the medial prefrontal cortex harvested from control, CUMS-MDD (mice with depression-like behaviors in CUMS group), Reward-MDD (mice with depression-like behaviors in CUMS-companion group), CUMS-resilience (resilient mice in CUMS group), Reward-resilience (resilient mice in CUMS-companion group) mice.Results The results provided evidence that accompanying with companion ameliorated CUMS-induced depression-like behaviors in mice. 45 differentially expressed genes (DEGs) are associated with depression-like behaviors, 8 DEGs are associated with resilience and 59 DEGs are associated with nature reward (companion) were identified. Furthermore, 196 differentially expressed miRNAs were found to be associated with companion. Based on the differentially expressed miRNAs and DEGs data, miRNA-mRNA network was established to be associated with companion.Conclusion Taken together, our data here provided a method to ameliorate depression-like behaviors, and numerous potential drug targets for the prevention or treatment of depression.

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