scholarly journals The interaction of chronic restraint stress and voluntary alcohol intake: Effects on spatial memory in male rats

Alcohol ◽  
2012 ◽  
Vol 46 (5) ◽  
pp. 499-504 ◽  
Author(s):  
Juan L. Gomez ◽  
Michael J. Lewis ◽  
Victoria N. Luine
Neuropeptides ◽  
2016 ◽  
Vol 60 ◽  
pp. 21-28 ◽  
Author(s):  
Jin Li ◽  
Han-Xia Li ◽  
Xiao-Jing Shou ◽  
Xin-Jie Xu ◽  
Tian-Jia Song ◽  
...  

2021 ◽  
Author(s):  
Tahmineh Mokhtari ◽  
AymanEl-Meghawry El-Kenawy ◽  
Li Hu

Abstract In this study, the effects of triiodothyronine (T3) were evaluated on the NLR family pyrin domain containing 3 (NLRP3) inflammasome complex formation in the rat's hippocampus with restraint stress-induced depressive-like behaviors.Thirty-six Wistar male rats were randomly allocated to following groups: Control, Model, and Model + T3. In the Model or Model+T3 group, a single dose of PBS or T3 was administered into the lateral ventricle. Depressive-like behaviors were induced by chronic restraint stress. The forced swimming (FST), tail suspension (TST), and open field (OFT) tests were used to investigate the depression. The rats were sacrificed, and brain tissues were stored for molecular and pathological evaluations. Chronic stress increased the immobility of rats in the Model group according to FST, TST, and OFT (P < 0.05). T3 significantly improved depressive-like behaviors (P < 0.05). The gene expression and protein level of hippocampal nuclear factor kappa B (NF-κB), NLRP3, apoptosis-associated speck-like protein (ASC), and Caspase-1 significantly increased in the Model group compared to the control group (P < 0.05). The reduced hippocampal levels of NF-κB, NLRP3, ASC, and Caspase-1 were observed in the T3 group compared to the Model group (P < 0.05). The Nissl staining of the CA1 region showed an increased number of dark neurons (P < 0.05) and reduced pyramidal layer thickness (P < 0.05) in the Model group. These histopathological alterations were changed by T3 administration compared to the Model group (P < 0.05). The findings confirmed the therapeutic effects of intraventricularly T3 on depressive-like behaviors induced by restraint stress via surviving pyramidal neurons of the CA1 region and inhibition of NF-κB/NLRP3 inflammasome pathway.


Author(s):  
Dool-Ri Oh ◽  
Yujin Kim ◽  
Sojeong Im ◽  
Kyo-Nyeo Oh ◽  
Jawon Shin ◽  
...  

Vaccinium bracteatum Thunb. Leaves (VBL) are a component of traditional herbal medicines. However, molecular mechanisms of VBL in stress-related memory impairment are still unclear. This study aimed to investigate the spatial memory improvement effects of VBL in an animal model of chronic restraint stress (CRS) by using Y maze test and identified possible protective mechanisms against oxidative stress inducers (e.g., corticosterone and hydrogen peroxide [H2O2]) in SH-SY5Y neuronal cells. VBL showed neuroprotective effects via reduced release of lactate dehydrogenase (LDH) in corticosterone or H2O2-induced cell death that was mediated through the regulation of cleaved caspase-3 and Nrf2 pathways. Furthermore, CRS-exposed mice were orally administered VBL (10, 50, 100, and 200 mg/kg) daily for 21 days. CRS-exposed mice treated with VBL showed significantly increased spontaneous alternation in short-term memory (STM) and long-term memory (LTM) trials, and number of total arm entries in LTM trials as measured by the Y maze test. Moreover, VBL (50, 100, and 200 mg/kg) decreased acetylcholinesterase (AChE) activity in the hippocampus (HC, [Formula: see text] < 0.01 and [Formula: see text] < 0.001, respectively) and prefrontal cortex (PFC). CRS-exposed mice treated with VBL had dramatically decreased total Tau and Tau phosphorylation in the synapse of the HC and PFC which might be mediated by the regulation of CaMKII and GSK3[Formula: see text] phosphorylation. Additionally, VBL reduced CRS-induced upregulation of N-methyl-D-aspartate (NMDA) receptor subunits (NMDAR1, 2A, and 2B). Thus, VBL exerts spatial memory improvement by regulating CRS-induced NMDA receptor neurotoxicity and Tau hyperphosphorylation.


2020 ◽  
Vol 21 (17) ◽  
pp. 6261 ◽  
Author(s):  
Paola Brivio ◽  
Giulia Sbrini ◽  
Giulia Corsini ◽  
Maria Serena Paladini ◽  
Giorgio Racagni ◽  
...  

Depression is a recurrent disorder, with about 50% of patients experiencing relapse. Exposure to stressful events may have an adverse impact on the long-term course of the disorder and may alter the response to a subsequent stressor. Indeed, not all the systems impaired by stress may normalize during symptoms remission, facilitating the relapse to the pathology. Hence, we investigated the long-lasting effects of chronic restraint stress (CRS) and its influence on the modifications induced by the exposure to a second hit on brain-derived neurotrophic factor (BDNF) signaling in the prefrontal cortex (PFC). We exposed adult male Sprague Dawley rats to 4 weeks of CRS, we left them undisturbed for the subsequent 3 weeks, and then we exposed animals to one hour of acute restraint stress (ARS). We found that CRS influenced the release of corticosterone induced by ARS and inhibited the ability of ARS to activate mature BDNF, its receptor Tropomyosin receptor kinase B (TRKB), and their associated intracellular cascades: the TRKB-PI3K-AKT), the MEK-MAPK/ERK, and the Phospholipase C γ (PLCγ) pathways, positively modulated by ARS in non-stressed animals. These results suggest that CRS induces protracted and detrimental consequences that interfere with the ability of PFC to cope with a challenging situation.


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