scholarly journals Arc/Arg3.1 protein expression in dorsal hippocampal CA1, a candidate event as a biomarker for the effects of exercise on chronic stress-evoked behavioral abnormalities

2017 ◽  
Vol 21 (4) ◽  
pp. 45-51
Author(s):  
Yea-Hyun Leem ◽  
Hyukki Chang
Andrologia ◽  
2021 ◽  
Author(s):  
Supatcharee Arun ◽  
Arada Chaiyamoon ◽  
Natthapol Lapyuneyong ◽  
Sudtida Bunsueb ◽  
Alexander Tsang‐Hsien Wu ◽  
...  

2020 ◽  
Vol 13 ◽  
pp. 100236
Author(s):  
Batsheva R. Rubin ◽  
Megan A. Johnson ◽  
Jared M. Berman ◽  
Ellen Goldstein ◽  
Vera Pertsovskaya ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 859 ◽  
Author(s):  
Huiling Chen ◽  
Qing Huang ◽  
Shunjia Zhang ◽  
Kaiqiang Hu ◽  
Wenxiang Xiong ◽  
...  

Major depressive disorder (MDD) is a chronic mental disorder characterized by mixed symptoms and complex pathogenesis. With long history of practical application, traditional Chinese medicine (TCM) offers many herbs for the treatment and rehabilitation of chronic disease. In this study, we developed a modified Chinese herbal formula using Panax ginseng, Angelica Sinensis, Polygala tenuifolia Willd, and Ziziphi spinosae Semen (PAPZ), based on an ancient TCM prescription. The antidepressant effects of PAPZ were investigated with a corticosterone (CORT) model of depression in mice. Our results showed that administration of PAPZ ameliorated depression-like phenotypes in the CORT model. An anatomic study showed that chronic PAPZ administration upregulated the protein expression of brain-derived neurotrophic factor (BDNF) in hippocampal tissue. The enzyme activity of superoxide dismutase was enhanced in hippocampal tissue, in line with a decreased malondialdehyde level. Taken together, these findings suggested that PAPZ has therapeutic effects in a mice depression model through increasing protein expression of BDNF and improving the anti-oxidation ability of the brain.


2014 ◽  
Vol 50 (3) ◽  
pp. 923-936 ◽  
Author(s):  
Matthias Schmitz ◽  
Catharina Greis ◽  
Philipp Ottis ◽  
Christopher J. Silva ◽  
Walter J. Schulz-Schaeffer ◽  
...  

2017 ◽  
Vol 1 ◽  
pp. 247054701772045 ◽  
Author(s):  
Mounira Banasr ◽  
Ashley Lepack ◽  
Corey Fee ◽  
Vanja Duric ◽  
Jaime Maldonado-Aviles ◽  
...  

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.


2005 ◽  
Vol 21 (5) ◽  
pp. 1304-1314 ◽  
Author(s):  
Vivi M. Heine ◽  
Jessica Zareno ◽  
Suharti Maslam ◽  
Marian Joëls ◽  
Paul J. Lucassen

2021 ◽  
Vol 28 (9) ◽  
pp. 319-328
Author(s):  
Jun Yokose ◽  
William D. Marks ◽  
Naoki Yamamoto ◽  
Sachie K. Ogawa ◽  
Takashi Kitamura

Temporal association learning (TAL) allows for the linkage of distinct, nonsynchronous events across a period of time. This function is driven by neural interactions in the entorhinal cortical–hippocampal network, especially the neural input from the pyramidal cells in layer III of medial entorhinal cortex (MECIII) to hippocampal CA1 is crucial for TAL. Successful TAL depends on the strength of event stimuli and the duration of the temporal gap between events. Whereas it has been demonstrated that the neural input from pyramidal cells in layer II of MEC, referred to as Island cells, to inhibitory neurons in dorsal hippocampal CA1 controls TAL when the strength of event stimuli is weak, it remains unknown whether Island cells regulate TAL with long trace periods as well. To understand the role of Island cells in regulating the duration of the learnable trace period in TAL, we used Pavlovian trace fear conditioning (TFC) with a 60-sec long trace period (long trace fear conditioning [L-TFC]) coupled with optogenetic and chemogenetic neural activity manipulations as well as cell type-specific neural ablation. We found that ablation of Island cells in MECII partially increases L-TFC performance. Chemogenetic manipulation of Island cells causes differential effectiveness in Island cell activity and leads to a circuit imbalance that disrupts L-TFC. However, optogenetic terminal inhibition of Island cell input to dorsal hippocampal CA1 during the temporal association period allows for long trace intervals to be learned in TFC. These results demonstrate that Island cells have a critical role in regulating the duration of time bridgeable between associated events in TAL.


eNeuro ◽  
2018 ◽  
Vol 5 (4) ◽  
pp. ENEURO.0104-18.2018 ◽  
Author(s):  
Andrew L. Eagle ◽  
Elizabeth S. Williams ◽  
Joseph A. Beatty ◽  
Charles L. Cox ◽  
Alfred J. Robison

Physiology ◽  
2019 ◽  
Vol 34 (2) ◽  
pp. 123-133 ◽  
Author(s):  
Kenny L. Chan ◽  
Flurin Cathomas ◽  
Scott J. Russo

Metabolic syndrome and major depression are two of the most common and debilitating disorders worldwide, occurring with significant rates of comorbidity. Recent studies have uncovered that each of these conditions is associated with chronic, low-grade inflammation. This is characterized by increased circulating pro-inflammatory cytokines, altered leukocyte population frequencies in blood, accumulation of immune cells in tissues including the brain, and activation of these immune cells. Cytokines that become elevated during obesity can contribute to the progression of metabolic syndrome by directly causing insulin resistance. During chronic stress, there is evidence that these cytokines promote depression-like behavior by disrupting neurotransmitter synthesis and signal transduction. Animal models of obesity and depression have revealed a bi-directional relationship whereby high-fat feeding and chronic stress synergize and exacerbate metabolic dysregulation and behavioral abnormalities. Although far from conclusive, emerging evidence suggests that inflammation in the central and peripheral immune system may link metabolic syndrome to major depressive disorder. In this review, we will synthesize available data supporting this view and identify critical areas for future investigation.


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