CUMS-induced Increase in ERα/ERβ Expression Is Associated with Dendritic Remodelling and Anxiety- and Depression-related Behaviour in Young Male Mice

The biological purpose of the stress response is to help the body to survive either some sort of attack or a serious illness like a stroke or heart attack. During the stress response glucocorticoids divert the bodies energy to the areas necessary for survival like the muscles and the brain and it shuts down the areas that are not necessary for survival like the digestive and immune systems (Sopolsky, 2009). Chronic Stress in this context, is to experience this physical effect on regular or long term basis. This has become a public health issue for humans because we experience this chronic biological response on a too frequent a basis for psychological reasons (Stress, 2008).

Stress is known to negatively impact health. Psychological responses, such as mood, emotion and coping, influence the way we perceive stress and the impact it has on the physiological response (Chida & Hamer, 2008). Past studies have used the hormone cortisol to test the stress response(Dickerson &

The nervous, endocrine, and immune systems share a close relationship critical to maintaining homeostasis during psychological and immune stress (Carlsson, Anneli, Ludvigsson, & Faresjö, 2014). Chronic stress, primarily mediated by the glucocorticoid cortisol, is associated with deleterious health outcomes and immune deficiency. However, acute stress is associated with protective health effects and immune enhancement. Stress has generally been regarded as adaptive when acute and short-term but maladaptive when chronic (Dhabhar, 2006; Carlsson, Anneli, Ludvigsson, & Faresjö, 2014; Johnson, Riley, Douglas, & Riis, 2013; Flinn and England, 2003; Wiegers, Reul, Holsboer, & de Kloet, 1994).

These adaptive mechanisms can become maladaptive if unresolved after precipitating events have passed, leading to interferences in emotional regulation (Liston, McEwen, & Casey, 2009; Juster et al., 2011). Imaging studies show alterations in the brain structures that assist in regulation of the stress response—the amygdala, hippocampus, and prefrontal cortex—due to prolonged exposure to stress (Carrion et al. 2010; Rao et al. 2010). The over activation of this fear circuitry in the brain can lead to distorted processing, contributing to depression (Thienkrua et al., 2006; Neria, Besser, Kiper, & Westphal, 2010; Rao et al., 2010), anxiety (Derryberry and Reed, 2002; Goldin et al., 2009; Graham and Milad, 2014), and mood impairments (Kobasa, 1979; Linehan, 1993; Haller and Miles, 2004). These cognitive changes can also contribute to insomnia, chronic pain, addictive disorders, impairment of immunity, and development of coping mechanisms such as smoking, use of alcohol or drugs, overeating, and other survival mechanisms (Raja, 2012). The allostatic load of a chronically over-activated hypothalamus-pituitary-adrenal system can lead to development of comorbid health conditions such as cardiovascular disease,

Adverse childhood experiences, for one, can potentially cause extreme childhood trauma and lead to chronic stress. Overloading the Hypothalamic pituitary adrenal axis (HPA axis) has the ability to cause recurring complexities and sends the body into an overdrive-like state. Paul Tough describes it as, “Overloading the HPA axis, especially in infancy and childhood, produces all kinds of serious and long-lasting negative effects—physical, psychological, and neurological.” (Tough, 13).

Firdaus Dhabhar gave a short lecture on August 19th, 2015 about the good effects that stress can have on our lives. I read two papers published by Dr. Dhabhar in the last five years, both concerning his research on the biological response of stress and how this can impact our daily lives as well as how it can be both detrimental and essential to good health. Each paper explored stress, one was more focused on the physical and the other focused on both the physical and the mental. Given my own project this summer, I was especially interested in the paper published by Aschbacher and colleagues in 2013 because they also explored cortisol reactivity to stress. While their project and my project looked at very different things in very different populations it was exciting to read more about cortisol and how people are exploring this hormone’s role in our stress

The physiological and behavioral effects of early life stress (ELS) on the developing and adult brain are a subject of great interest in the field of neuroscience today. The ability to delineate the mechanisms and structures that are affected during postnatal exposure to chronic stress has the potential to provide invaluable insight into the development of a multitude of neuropsychiatric disorders. While we have come to understand a few of the mechanisms involved in many of these illnesses – such as the significance of the serotonin (5-hydroxytryptamine, 5-HT) neurotransmitter in many depression cases – the complex nature of these disorders and our ability to effectively treat them remains elusive. Such an understanding of how the brain adapts and differentially develops as a result of chronic stress, particularly in early life, may also be able to broaden our understanding of the way in which the brain codes and responds to a variety of emotional triggers.

Stress can be broadly defined as any external and internal events that affects an organism’s well being. In attempt to maintain homeostasis, the body will respond to the psychological stress by modifying physiological processes (Nargund, 2015). Psychological stress is a number of emotional events that interrupts homeostasis. The disruption of homeostasis can affect many biological systems, such as metabolism, vascular function, tissue repair, nervous system and reproductive system. Both emotional and physical stress can have a negative impact on human reproductive function (Cousineau, 2007; Jakobovits et al, 2002). Therefore, it is very important to know how to cope with stress when experiencing life events that are very stressful. My presentation

Hammer, M., & Steptoe., A, (20120. Cortisol responses to Mental Stress and Hypertension. The journal of clinical Endocrinology and Metabolism, 97(1), E21-E34. doi: https//dx.doi.org/10.1210/ic-2011-2132

Stress is one of the most important factors responsible for depressive disorders [11]. The chronic mild stress (CMS) model, a widely used rodent model of depression, consists of repeated exposure to an array of varying and unpredictable, mild stressors and it induces changes in hypothalamic-pituitary-adrenal (HPA) axis Katz et al. 1981Vollmayr B, Henn FA (2003)

Acute stress responses in young, healthy individuals may be adaptive and typically do not impose a health burden.

On the other hand, allostasis is different that regular homeostasis proposes maintenance of stability outside of the normal homeostatic range where an organism must vary all the parameters of its physiological systems to match them appropriately to chronic demands (i.e., reset the system parameters to a new set points). The main hormonal mediators of the stress response in this situation are cortisol and epinephrine (adrenaline). They have both protective and damaging effects on the body. Allostasis implies that many, if not all, physiological functions are mobilized or suppresses as reflected in a cascade of brain-organism interactions overriding local regulation. In the short run, they are essential for adaption, maintenance of homeostasis,

Anxiety is a common consequence of chronic stress. In humans, stressful life events may lead to anxiety even in the absence of a chronic physiological stress response [13]. Many studies have been conducted to identify the role of different factors that contribute to the development of depression and anxiety [A,B].It has been reported that decrease anxiety related behavior in humans and animals.( ?) Among trusty models of depression, chronic mild stress (CMS) model of

Chronic stress can also interfere with the body’s immune system directly through hormonal changes. Glucocorticoids-a hormone

Adverse early life experience affects physiological and behavioral development, leading to differences in life-history outcomes. One key component is the relationship between the developing sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis. Recent studies have suggested an association between early life adversity (ELA) and asymmetry in cortisol (a measure of HPA axis activation) and salivary alpha-amylase (a correlate of SNS activation) responses to stress among human children, but to my knowledge there have been no studies of such a relationship in nonhumans. Here, I investigate the responses of these analytes to non-stressful and stressful events in a cohort of free-ranging juvenile rhesus macaques (Macaca mulatta) on Cayo Santiago, Puerto Rico. Behavioral data collected on maternal rejection and abuse during each juvenile’s first three months of life was used to determine individual ELA categories. Saliva samples were collected from juveniles during both “low stress” and “high stress” states. High ELA juveniles were found to exhibit blunted cortisol responsiveness during “high stress” situations compared to moderate and low ELA juveniles. These juveniles were also found to have the highest “low stress” cortisol levels of the three groups. Further, sAA output was higher overall during “high stress” states than during “low stress” states, but did not significantly differ among the three ELA categories. Cortisol and sAA values