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Hormones Stress and the Brain

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Mechanisms of stress in the brain. The impact of stress on body function: A review. How does the brain deal with cumulative stress? A review with focus on developmental stress, HPA axis function and hippocampal structure in humans. Stress is believed to play an important role in the pathogenesis of major depressive disorder (MDD). Currently, there is much debate about the effect of early life adversity and its potential associations with the specific course of illness, long-lasting emotional problems (Carboni et al., 2010, Heim and N. C., 2001, Mann and Currier, 2010), and hippocampal volumetric changes (Chen et al., 2010). Chronic stress can increase rates of depression in susceptible individuals but the detailed pathophysiology underlying this process remains unknown (Tsankova et al., 2006).

In the following paragraphs of this section we will describe normal stress responses and the abnormal stress responses commonly found in MDD. How our bodies respond to stressors to a large extent determines our overall health. The brain is the main regulatory organ for stress responses. CRH is the main brain peptide involved in the activation of the HPA axis. Effects of early life stress on cognitive and affective function: an integrated review of human literature. Accident Compensation Corporation (2008) Sexual abuse and mental injury: practice guidelines for Aotearoa/New Zealand. ACC, Wellington Google Scholar Admon R, Lubin G, Stern O, Rosenberg K, Sela L, Ben-Ami H et al (2009) Human vulnerability to stress depends on amygdala’s predisposition and hippocampal plasticity. Proc Natl Acad Sci USA 106:14120–14125PubMed CAS Google Scholar Adolphs R (2002) Neural systems for recognizing emotion.

Curr Opin Neurobiol 12:169–177PubMed CAS Google Scholar Anda R, Croft JB, Felitti V, Nordenberg D, Giles W, Wiliamson DF et al (1999) Adverse childhood experiences and smoking during adolescence and adulthood. JAMA 228:1652–1658 Google Scholar Anda R, Felitti V, Bremner J, Walker J, Whitfield C, Perry B et al (2006) The enduring effects of abuse and related adverse experiences in childhood.

A Comprehensive Overview on Stress Neurobiology: Basic Concepts and Clinical Implications | Behavioral Neuroscience. Introduction Stress is recognized as an important issue in basic and clinical neuroscience research (de Kloet et al., 2005a; McEwen et al., 2015). Although this physiological phenomenon is fundamental to survival, it is also strongly related to several brain disorders including, depression, anxiety, post-traumatic stress disorder (Ruiz et al., 2007; Heim et al., 2008; Martin et al., 2009; Walsh, 2011; Saveanu and Nemeroff, 2012; Nemeroff, 2016) accordingly to the International Classification of Diseases, 10th edition (ICD-10).

Research focusing on the complexity of stress is still challenging, but several studies in animals and humans have made substantial contributions to its progress in recent years, as reviewed by Hariri and Holmes (2015). However, it is crucial to provide more meaningful advances in the stress field by means of a translational approach, integrating basic knowledge and clinical practice. History of Stress Research Figure 1. Neuroanatomy Figure 2. Physical Stressors. Preconception Paternal Stress in Rats Alters Brain and Behavior in Offspring - PubMed. Whereas environmental challenges during gestation have been repeatedly shown to alter offspring brain architecture and behavior, exploration examining the consequences of paternal preconception experience on offspring outcome is limited.

The goal of this study was to examine the effects of preconception paternal stress (PPS) on cerebral plasticity and behavior in the offspring. Several behavioral assays were performed on offspring between postnatal days 33 (P33) and 101 (P101). Following behavioral testing, the brains were harvested and dendritic morphology (dendritic complexity, length, and spine density) were examined on cortical pyramidal cells in medial prefrontal cortex (mPFC), orbital frontal cortex (OFC), parietal cortex (Par1), and the CA1 area of the hippocampus. As anticipated, behavior was altered on both the activity box assay and elevated plus maze and performance was impaired in the Whishaw tray reaching task. Chronic Variable Stress Is Responsible for Lipid and DNA Oxidative Disorders and Activation of Oxidative Stress Response Genes in the Brain of Rats - PubMed.

Chronic environmental stress is associated with reactive oxygen species (ROS) overproduction and the pathogenesis of depression. The purpose of this study was to evaluate biochemical and molecular changes associated with ROS generation in the brains of rats submitted to chronic variable stress. Male Wistar rats (50-55 days old, weighing 200-250 g) were divided in two groups (n = 10): control and stressed. Rats in the stressed group were exposed to stress conditions for 40 days. The animals were decapitated and the brain samples were collected.

In prefrontal cortex, we measured the following biochemical parameters: lipid peroxidation and concentration of glutathione-GSH, GSSG, GSH/GSSG ratio, glutathione peroxidase, and glutathione reductase activities. In the hippocampus marker of DNA, oxidative damage and expression of DNA-repairing genes (Ogg1, MsrA) and gene-encoding antioxidative transcriptional factor (Nrf2) were determined. Physiology and Neurobiology of Stress and Adaptation: Central Role of the Brain - PubMed. The brain is the key organ of the response to stress because it determines what is threatening and, therefore, potentially stressful, as well as the physiological and behavioral responses which can be either adaptive or damaging. Stress involves two-way communication between the brain and the cardiovascular, immune, and other systems via neural and endocrine mechanisms. Beyond the "flight-or-fight" response to acute stress, there are events in daily life that produce a type of chronic stress and lead over time to wear and tear on the body ("allostatic load").

Yet, hormones associated with stress protect the body in the short-run and promote adaptation ("allostasis"). The brain is a target of stress, and the hippocampus was the first brain region, besides the hypothalamus, to be recognized as a target of glucocorticoids. Stress and stress hormones produce both adaptive and maladaptive effects on this brain region throughout the life course. The Dynamics of the Stress Neuromatrix - PubMed. The Effects of Stress on Brain and Adrenal Stem Cells - PubMed. The brain and adrenal are critical control centers that maintain body homeostasis under basal and stress conditions, and orchestrate the body's response to stress. It is noteworthy that patients with stress-related disorders exhibit increased vulnerability to mental illness, even years after the stress experience, which is able to generate long-term changes in the brain's architecture and function.

High levels of glucocorticoids produced by the adrenal cortex of the stressed subject reduce neurogenesis, which contributes to the development of depression. In support of the brain-adrenal connection in stress, many (but not all) depressed patients have alterations in the components of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis, with enlarged adrenal cortex and increased glucocorticoid levels. Decoding Microglia Responses to Psychosocial Stress Reveals Blood-Brain Barrier Breakdown That May Drive Stress Susceptibility - PubMed. How the Brain Connects in Response to Acute Stress: A Review at the Human Brain Systems Level - PubMed. Brain Mineralocorticoid Receptors and Resilience to Stress - PubMed. Involvement of Activated Brain Stress Responsive Systems in Excessive and "Relapse" Alcohol Drinking in Rodent Models: Implications for Therapeutics - PubMed. Addictive diseases, including addiction to alcohol, pose massive public health costs. Addiction is a chronic relapsing disease caused by both the direct effects induced by drugs and persistent neuroadaptations at the molecular, cellular, and behavioral levels.

These drug-type specific neuroadaptations are brought on largely by the reinforcing effects of drugs on the central nervous system and environmental stressors. Results from animal experiments have demonstrated important interactions between alcohol and stress-responsive systems. Addiction to specific drugs such as alcohol, psychostimulants, and opioids shares some common direct or downstream effects on the brain's stress-responsive systems, including arginine vasopressin and its V1b receptors, dynorphin and the κ-opioid receptors, pro-opiomelanocortin/β-endorphin and the μ-opioid receptors, and the endocannabinoids. Effect of Stress on Structural Brain Asymmetry - PubMed. The Stressed Brain of Humans and Rodents - PubMed.

The Effects of Childhood Maltreatment on Brain Structure, Function and Connectivity - PubMed. Brain Metabolism in Health, Aging, and Neurodegeneration - PubMed. The Microbiota-Gut-Brain Axis as a Key Regulator of Neural Function and the Stress Response: Implications for Human and Animal Health - PubMed. The brain-gut-microbiota axis comprises an extensive communication network between the brain, the gut, and the microbiota residing there. Development of a diverse gut microbiota is vital for multiple features of behavior and physiology, as well as many fundamental aspects of brain structure and function. Appropriate early-life assembly of the gut microbiota is also believed to play a role in subsequent emotional and cognitive development. If the composition, diversity, or assembly of the gut microbiota is impaired, this impairment can have a negative impact on host health and lead to disorders such as obesity, diabetes, inflammatory diseases, and even potentially neuropsychiatric illnesses, including anxiety and depression.

Therefore, much research effort in recent years has focused on understanding the potential of targeting the intestinal microbiota to prevent and treat such disorders. Adapting to Stress: Understanding the Neurobiology of Resilience - PubMed. There is significant variation in the way individuals react and respond to extreme stress and adversity. While some individuals develop psychiatric conditions such as posttraumatic stress disorder or major depressive disorder, others recover from stressful experiences without displaying significant symptoms of psychological ill-health, demonstrating stress-resilience. To understand why some individuals exhibit characteristics of a resilient profile, the interplay between neurochemical, genetic, and epigenetic processes over time needs to be explained.

In this review, we examine the hormones, neuropeptides, neurotransmitters, and neural circuits associated with resilience and vulnerability to stress-related disorders. We debate how this increasing body of knowledge could also be useful in the creation of a stress-resilient profile. Keywords: PTSD; biological markers; depression;; resilience; uncontrollable stress. The Programming of the Social Brain by Stress During Childhood and Adolescence: From Rodents to Humans - PubMed. The quality and quantity of social experience is fundamental to an individual's health and well-being. Early life stress is known to be an important factor in the programming of the social brain that exerts detrimental effects on social behaviors.

The peri-adolescent period, comprising late childhood and adolescence, represents a critical developmental window with regard to the programming effects of stress on the social brain. Here, we discuss social behavior and the physiological and neurobiological consequences of stress during peri-adolescence in the context of rodent paradigms that model human adversity, including social neglect and isolation, social abuse, and exposure to fearful experiences. Furthermore, we discuss peri-adolescent stress as a potent component that influences the social behaviors of individuals in close contact with stressed individuals and that can also influence future generations. Corticosteroids and the Brain - PubMed. The brain is continuously exposed to varying levels of adrenal corticosteroid hormones such as corticosterone in rodents and cortisol in humans. Natural fluctuations occur due to ultradian and circadian variations or are caused by exposure to stressful situations. Brain cells express two types of corticosteroid receptors, i.e. mineralocorticoid and glucocorticoid receptors, which differ in distribution and affinity.

These receptors can mediate both rapid non-genomic and slow gene-mediated neuronal actions. As a consequence of these factors, natural (e.g. stress-induced) shifts in corticosteroid level are associated with a complex mosaic of time- and region-dependent changes in neuronal activity. A series of experiments in humans and rodents have revealed that these time- and region-dependent cellular characteristics are also reflected in distinct cognitive patterns after stress. Keywords: corticosterone; epilepsy; glucocorticoid receptor; hippocampus; mineralocorticoid receptor.

Intermittent Metabolic Switching, Neuroplasticity and Brain Health - PubMed. The Role of Brain Reward Pathways in Stress Resilience and Health - PubMed. Stress Response, Brain Noradrenergic System and Cognition - PubMed. How the Brain Connects in Response to Acute Stress: A Review at the Human Brain Systems Level - PubMed. Stress-induced Perinatal and Transgenerational Epigenetic Programming of Brain Development and Mental Health - PubMed. Research efforts during the past decades have provided intriguing evidence suggesting that stressful experiences during pregnancy exert long-term consequences on the future mental wellbeing of both the mother and her baby.

Recent human epidemiological and animal studies indicate that stressful experiences in utero or during early life may increase the risk of neurological and psychiatric disorders, arguably via altered epigenetic regulation. Epigenetic mechanisms, such as miRNA expression, DNA methylation, and histone modifications are prone to changes in response to stressful experiences and hostile environmental factors. Altered epigenetic regulation may potentially influence fetal endocrine programming and brain development across several generations. Only recently, however, more attention has been paid to possible transgenerational effects of stress. Stress and the Gut Microbiota-Brain Axis - PubMed. Stress is a nonspecific response of the body to any demand imposed upon it, disrupting the body homoeostasis and manifested with symptoms such as anxiety, depression or even headache. These responses are quite frequent in the present competitive world. The aim of this review is to explore the effect of stress on gut microbiota.

First, we summarize evidence of where the microbiota composition has changed as a response to a stressful situation, and thereby the effect of the stress response. Likewise, we review different interventions that can modulate microbiota and could modulate the stress according to the underlying mechanisms whereby the gut-brain axis influences stress. Finally, we review both preclinical and clinical studies that provide evidence of the effect of gut modulation on stress. An Unpredictable Chronic Mild Stress Protocol for Instigating Depressive Symptoms, Behavioral Changes and Negative Health Outcomes in Rodents.

Chronic, unresolved stress is a major risk factor for the development of clinical depression. While many preclinical models of stress-induced depression have been reported, the unpredictable chronic mild stress (UCMS) protocol is an established translationally-relevant model for inducing behavioral symptoms commonly associated with clinical depression, such as anhedonia, altered grooming behavior, and learned helplessness in rodents. The UCMS protocol also induces physiological (e.g., hypercortisolemia, hypertension) and neurological (e.g., anhedonia, learned helplessness) changes that are clinically associated with depression. Importantly, UCMS-induced depressive symptoms can be ameliorated through chronic, but not acute, treatment with common SSRIs.

As such, the UCMS protocol offers many advantages over acute stress protocols or protocols that utilize more extreme stressors. Brain structure adaptation to stress TINS 2012. Stress acts cumulatively to precipitate Alzheimer... [J Neurosci. 2011. Stress Cortisol Connection. Stress May Cause The Brain To Become Disconnected. Effect of chronic stress on the structural plasticity in the brain. How the Mind Works | Video channel on TED.com.

Does Stress Change the Brain? Life Stress - How To Stop Life Stress Before It Becomes Severe. The Definitive Guide to Stress, Cortisol, and the Adrenals: When ‘Fight or Flight’ Meets the Modern World. Cortisol and Stress: How Cortisol Affects Your Body, and How To Stay Healthy in the Face of Stress. Behavioral problems linked to cortisol levels: Study finds intervention needed as soon as behavioral problems appear. Cortisol.