scholarly journals Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain

2015 ◽  
Vol 28 (1) ◽  
pp. 18-31 ◽  
Author(s):  
Jeremy Duncan ◽  
Niping Wang ◽  
Xiao Zhang ◽  
Shakevia Johnson ◽  
Sharonda Harris ◽  
...  
Keyword(s):  
Cell Death ◽  
Rat Brain ◽  
Social Stress ◽  
Chronic Social Stress ◽  
A Cell

scholarly journals Chronic Social Stress Alters Levels of Corticotropin-Releasing Factor and Arginine Vasopressin mRNA in Rat Brain

1997 ◽  
Vol 17 (12) ◽  
pp. 4895-4903 ◽  
Author(s):  
David S. Albeck ◽  
Christina R. McKittrick ◽  
D. Caroline Blanchard ◽  
Robert J. Blanchard ◽  
Julia Nikulina ◽  
...  
Keyword(s):  
Rat Brain ◽  
Arginine Vasopressin ◽  
Social Stress ◽  
Corticotropin Releasing Factor ◽  
Chronic Social Stress

Stress-reactivity in winner and loser rats after chronic social stress

2010 ◽  
Author(s):  
V. Paholchenko ◽  
E. Tukalenko ◽  
M. Makarchuk
Keyword(s):  
Social Stress ◽  
Stress Reactivity ◽  
Chronic Social Stress

Individual Differences in Response to Chronic Social Stress: Behavioral, Endocrine and Immune Profiles

2008 ◽  
Author(s):  
Eneritz Gomez ◽  
Amaia Arregi ◽  
Garikoitz Beitia ◽  
Oscar Vegas ◽  
Arantza Azpiroz ◽  
...  
Keyword(s):  
Individual Differences ◽  
Social Stress ◽  
Chronic Social Stress

Lasting effects of chronic social stress in mice: Impact of antidepressant treatment

2009 ◽  
Vol 42 (05) ◽  
Author(s):  
SH Scharf ◽  
V Sterlemann ◽  
C Liebl ◽  
K Ganea ◽  
P Weber ◽  
...  
Keyword(s):  
Social Stress ◽  
Antidepressant Treatment ◽  
Chronic Social Stress

Citalopram abolishes depressive-like symptoms evoked by chronic social stress in rats

2005 ◽  
Vol 38 (05) ◽  
Author(s):  
U Havemann-Reinecke ◽  
R Rygula ◽  
N Abumaria ◽  
E Rüther ◽  
C Hiemke ◽  
...  
Keyword(s):  
Social Stress ◽  
Chronic Social Stress

A Cell Death Pathway Induced by Antibody-Mediated Cross-Linking of CD45 on Lymphocytes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 421-440 ◽  
Author(s):  
Ann-Muriel Steff ◽  
Marylene Fortin ◽  
Fabianne Philippoussis ◽  
Sylvie Lesage ◽  
Chantal Arguin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Linking ◽  
Cell Death Pathway ◽  
A Cell

Structural Changes of Rats Skin under the Influence of Chronic Social Stress

2017 ◽  
Vol 2 (5) ◽  
pp. 26-29
Author(s):  
M. I. Zavgorodnyaya ◽  
◽  
V. V. Smagin ◽  
L. V. Makyeyeva ◽  
O. G. Alieva ◽  
...  
Keyword(s):  
Social Stress ◽  
Structural Changes ◽  
Chronic Social Stress

Use of Both Fluoro-Jade B and Hematoxylin and Eosin to Detect Cell Death in the Juvenile Rat Brain Exposed to NMDA-Receptor Antagonists or GABA-Receptor Agonists in Safety Assessment

2021 ◽  
pp. 019262332110077
Author(s):  
Catherine A. Picut ◽  
Odete R. Mendes ◽  
David S. Weil ◽  
Sarah Davis ◽  
Cynthia Swanson
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Rat Brain ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Nmda Receptor Antagonists ◽  
Neonatal Rats ◽  
Receptor Antagonists ◽  
Fluoro Jade B ◽  
Hematoxylin And Eosin

Administration of pediatric anesthetics with N-methyl D-aspartate (NMDA)-receptor antagonist and/or γ-aminobutyric acid (GABA) agonist activities may result in neuronal degeneration and/or neuronal cell death in neonatal rats. Evaluating pediatric drug candidates for this potential neurotoxicity is often part of overall preclinical new drug development strategy. This specialized assessment may require dosing neonatal rats at postnatal day 7 at the peak of the brain growth spurt and evaluating brain tissue 24 to 48 hours following dosing. The need to identify methods to aid in the accurate and reproducible detection of lesions associated with this type of neurotoxic profile is paramount for meeting the changing needs of neuropathology assessment and addressing emerging challenges in the neuroscience field. We document the use of Fluoro-Jade B (FJB) staining, to be used in conjunction with standard hematoxylin and eosin staining, to detect acute neurodegeneration and neuronal cell death that can be caused by some NMDA-receptor antagonists and/or GABA agonists in the neonatal rat brain. The FJB staining is simple, specific, and sensitive and can be performed on brain specimens from the same cohort of animals utilized for standard neurotoxicity assessment, thus satisfying animal welfare recommendations with no effect on achievement of scientific and regulatory goals.

scholarly journals Mitochondria and Pharmacologic Cardiac Conditioning—At the Heart of Ischemic Injury

2021 ◽  
Vol 22 (6) ◽  
pp. 3224
Author(s):  
Christopher Lotz ◽  
Johannes Herrmann ◽  
Quirin Notz ◽  
Patrick Meybohm ◽  
Franz Kehl
Keyword(s):  
Cell Death ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Research Field ◽  
Calcium Handling ◽  
Control Mechanisms ◽  
Intrinsic Resistance ◽  
Atp Production ◽  
Cardiac Conditioning ◽  
A Cell

Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.

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