scholarly journals Early-life stress origins of gastrointestinal disease: animal models, intestinal pathophysiology, and translational implications

2015 ◽  
Vol 309 (12) ◽  
pp. G927-G941 ◽  
Author(s):  
Calvin S. Pohl ◽  
Julia E. Medland ◽  
Adam J. Moeser
Keyword(s):  
Animal Models ◽  
Life Stress ◽  
Early Life ◽  
Disease Susceptibility ◽  
Gastrointestinal Disease ◽  
Adult Life ◽  
Early Life Stress ◽  
Early Postnatal Development ◽  
Disease States ◽  
Fundamental Understanding

Early-life stress and adversity are major risk factors in the onset and severity of gastrointestinal (GI) disease in humans later in life. The mechanisms by which early-life stress leads to increased GI disease susceptibility in adult life remain poorly understood. Animal models of early-life stress have provided a foundation from which to gain a more fundamental understanding of this important GI disease paradigm. This review focuses on animal models of early-life stress-induced GI disease, with a specific emphasis on translational aspects of each model to specific human GI disease states. Early postnatal development of major GI systems and the consequences of stress on their development are discussed in detail. Relevant translational differences between species and models are highlighted.

scholarly journals Animal models of early life stress: Implications for understanding resilience

2010 ◽  
Vol 52 (5) ◽  
pp. 402-410 ◽  
Author(s):  
David M. Lyons ◽  
Karen J. Parker ◽  
Alan F. Schatzberg
Keyword(s):  
Animal Models ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress

scholarly journals Does epigenetic ‘memory’ of early-life stress predispose to chronic pain in later life? A potential role for the stress regulator FKBP5

2019 ◽  
Vol 374 (1785) ◽  
pp. 20190283 ◽  
Author(s):  
S. M. Géranton
Keyword(s):  
Chronic Pain ◽  
Life Stress ◽  
Early Life ◽  
Potential Role ◽  
Adult Life ◽  
Early Life Stress ◽  
Later Life ◽  
Stress Axis ◽  
Evolutionarily Conserved ◽  
Early Life Events

Animal behaviours are affected not only by inherited genes but also by environmental experiences. For example, in both rats and humans, stressful early-life events such as being reared by an inattentive mother can leave a lasting trace and affect later stress response in adult life. This is owing to a chemical trace left on the chromatin attributed to so-called epigenetic mechanisms. Such an epigenetic trace often has consequences, sometimes long-lasting, on the functioning of our genes, thereby allowing individuals to rapidly adapt to a new environment. One gene under such epigenetic control is FKBP5 , the gene that encodes the protein FKPB51, a crucial regulator of the stress axis and a significant driver of chronic pain states. In this article, we will discuss the possibility that exposure to stress could drive the susceptibly to chronic pain via epigenetic modifications of genes within the stress axis such as FKBP5 . The possibility that such modifications, and therefore, the susceptibility to chronic pain, could be transmitted across generations in mammals and whether such mechanisms may be evolutionarily conserved across phyla will also be debated. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

Early life stress paradigms in rodents: potential animal models of depression?

2010 ◽  
Vol 214 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Mathias V. Schmidt ◽  
Xiao-Dong Wang ◽  
Onno C. Meijer
Keyword(s):  
Animal Models ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Animal Models Of Depression

scholarly journals Maternal Separation Induces Sex-Specific Differences in Sensitivity to Traumatic Stress

2021 ◽  
Vol 15 ◽  
Author(s):  
Dayan Knox ◽  
Stephanie A. Stout-Oswald ◽  
Melissa Tan ◽  
Sophie A. George ◽  
Israel Liberzon
Keyword(s):  
Risk Factors ◽  
Sex Differences ◽  
Animal Models ◽  
Traumatic Stress ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Female Rats ◽  
Male Rats

Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder with a high economic burden. Two risk factors for increasing the chances of developing PTSD are sex (being female) and early life stress. These risk factors suggest that early life stress-induced changes and sex differences in emotional circuits and neuroendocrinological systems lead to susceptibility to traumatic stress. Exploring mechanisms via which stress leads to specific effects can be accomplished in animal models, but reliable animal models that allow for an examination of how early life stress interacts with sex to increase susceptibility to traumatic stress is lacking. To address this, we examined the effects of early life stress [using the maternal separation (MS) model] and late adolescence/early adult traumatic stress [using the single prolonged stress (SPS) model] on startle reactivity, anxiety-like behavior in the open field (OF), and basal corticosterone levels in male and female rats. Female rats exposed to MS and SPS (MS/SPS) showed enhanced startle reactivity relative to MS/control female rats. Enhanced startle reactivity was not observed in MS/SPS male rats. Instead, non-maternally separated male rats that were exposed to SPS showed enhanced startle reactivity relative to controls. Female rats had enhanced locomotor activity in the OF and higher basal corticosterone levels in comparison to males, but measures in the OF and basal corticosterone were not affected by MS or SPS. Overall the results suggest that the combined MS and SPS models can be used to explore how changes in maternal care during infancy lead to sex differences in sensitivity to the effects of traumatic stress as adolescents and adults.

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