S.23.03 Genetic and epigenetic moderator of the first transcriptome response to stress: importance for stress-related psychiatric disorders?

2015 ◽  
Vol 25 ◽  
pp. S144-S145
Author(s):  
E. Binder
Keyword(s):  
Psychiatric Disorders ◽  
Response To Stress ◽  
Transcriptome Response

scholarly journals Genetic Differences in the Immediate Transcriptome Response to Stress Predict Risk-Related Brain Function and Psychiatric Disorders

Neuron ◽  
2015 ◽  
Vol 86 (5) ◽  
pp. 1189-1202 ◽  
Author(s):  
Janine Arloth ◽  
Ryan Bogdan ◽  
Peter Weber ◽  
Goar Frishman ◽  
Andreas Menke ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Brain Function ◽  
Genetic Differences ◽  
Response To Stress ◽  
Transcriptome Response

scholarly journals Regulation of dopamine system responsivity and its adaptive and pathological response to stress

2015 ◽  
Vol 282 (1805) ◽  
pp. 20142516 ◽  
Author(s):  
Pauline Belujon ◽  
Anthony A. Grace
Keyword(s):  
Stress Response ◽  
Psychiatric Disorders ◽  
Crucial Role ◽  
Current Knowledge ◽  
Pathological Response ◽  
Psychiatric Diseases ◽  
Dopamine System ◽  
Norepinephrine System ◽  
Response To Stress

Although, historically, the norepinephrine system has attracted the majority of attention in the study of the stress response, the dopamine system has also been consistently implicated. It has long been established that stress plays a crucial role in the pathogenesis of psychiatric disorders. However, the neurobiological mechanisms that mediate the stress response and its effect in psychiatric diseases are not well understood. The dopamine system can play distinct roles in stress and psychiatric disorders. It is hypothesized that, even though the dopamine (DA) system forms the basis for a number of psychiatric disorders, the pathology is likely to originate in the afferent structures that are inducing dysregulation of the DA system. This review explores the current knowledge of afferent modulation of the stress/DA circuitry, and presents recent data focusing on the effect of stress on the DA system and its relevance to psychiatric disorders.

scholarly journals The role of m6A-RNA methylation in stress response regulation

2017 ◽  
Author(s):  
Mareen Engel ◽  
Simone Röh ◽  
Carola Eggert ◽  
Paul M. Kaplick ◽  
Lisa Tietze ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Synaptic Plasticity ◽  
Stress Response ◽  
Depressive Disorder ◽  
Psychiatric Disorders ◽  
Fear Memory ◽  
Receptor Activation ◽  
Major Depressive ◽  
Rna Methylation ◽  
Transcriptome Response

SummaryN6-Methyladenosine (m6A) is an abundant internal RNA modification that regulates transcript processing and translation. The regulation of brain m6A by stressful stimuli in vivo and its role in the stress response are currently unknown.Here, we provide a detailed analysis of the stress-epitranscriptome using m6A-Seq, global and gene-specific m6A measurements. We show that stress exposure and glucocorticoids alter m6A and its regulatory network in a region- and time-specific manner. We demonstrate that depletion of the methyltransferase Mettl3 and the demethylase Fto in adult neurons increases fear memory, and alters the transcriptome response to fear as well as synaptic plasticity. Finally, we report that regulation of m6A is impaired in major depressive disorder patients following glucocorticoid receptor activation.Our findings indicate that brain m6A represents a novel layer of complexity in gene expression regulation after stress and that dysregulation of the m6A-response may contribute to the pathophysiology of stress-related psychiatric disorders.Highlightsm6A RNA methylation in adult mouse brain is regulated by stressBrain m6A levels are temporally and spatially regulated by stressMettl3 and Fto-KO alter fear memory, transcriptome response and synaptic plasticityThe m6A-glucocorticoid-response is impaired in major depressive disorder patientseTOC blurbEngel et al. demonstrate a brain-area-specific and time-dependent role for the mRNA modification, m6A, in stress-response regulation. Manipulating m6A-enzymes alters fear-memory, transcriptome-response and synaptic-plasticity. Altered m6A dynamics in depressed patients suggest an involvement of m6A-modifications in stress-related psychiatric disorders.

scholarly journals The Habenula in the Link Between ADHD and Mood Disorder

2021 ◽  
Vol 15 ◽  
Author(s):  
Young-A Lee ◽  
Yukiori Goto
Keyword(s):  
Mood Disorder ◽  
Psychiatric Disorders ◽  
Neurodevelopmental Disorder ◽  
Psychomotor Retardation ◽  
Testable Hypothesis ◽  
Childhood Onset ◽  
Genetic Studies ◽  
Hyperactivity Disorder ◽  
Response To Stress ◽  
New Perspective

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset, neurodevelopmental disorder, whereas major depressive disorder (MDD) is a mood disorder that typically emerges in adulthood. Accumulating evidence suggests that these seemingly unrelated psychiatric disorders, whose symptoms even appear antithetical [e.g., psychomotor retardation in depression vs. hyperactivity (psychomotor acceleration) in ADHD], are in fact associated with each other. Thus, individuals with ADHD exhibit high comorbidity with MDD later in life. Moreover, genetic studies have shown substantial overlaps of susceptibility genes between ADHD and MDD. Here, we propose a novel and testable hypothesis that the habenula, the epithalamic brain region important for the regulation of monoamine transmission, may be involved in both ADHD and MDD. The hypothesis suggests that an initially hypoactive habenula during childhood in individuals with ADHD may undergo compensatory changes during development, priming the habenula to be hyperactive in response to stress exposure and thereby increasing vulnerability to MDD in adulthood. Moreover, we propose a new perspective on habenular deficits in psychiatric disorders that consider the habenula a neural substrate that could explain multiple psychiatric disorders.

Predisposition to Depression: The Role of Attachment

2003 ◽  
Vol 37 (2) ◽  
pp. 219-225 ◽  
Author(s):  
Josephine Beatson ◽  
Suzanna Taryan
Keyword(s):  
Psychiatric Disorders ◽  
Patient Group ◽  
Hpa Axis ◽  
Early Life ◽  
Life Experience ◽  
Adverse Life Events ◽  
Relational Experiences ◽  
Early Life Experience ◽  
Response To Stress

Objective: To examine the hypothesis that adverse early relational experiences causing activation of the hypophysial-pituitary-adrenal (HPA) axis during critical early stages of development can predispose to depression. Patients thus affected are likely to manifest insecure patterns of attachment in close relationships and are vulnerable to depression after adverse life events. Method: The literature pertaining to sensitization of the HPA axis in early life and the neurobiology of attachment is examined. Results: Adverse early relational experiences can result in activation of the HPA axis, causing sensitization of depression pathways in the brain. Secure attachment acts as a buffer against HPA activation in response to stress. Infants with insecure attachment lack this buffering effect and may be predisposed to depression and other psychiatric disorders in response to psychosocial stressors. Conclusions: There is a patient group predisposed to depression on the basis of adverse early life experience. In these cases, the neurobiology of attachment offers a means of integrating findings concerning sensitization of the HPA axis in infancy, the effects of early life experience on brain development, and predisposition to depression and other psychiatric disorders. These findings have important implications for the development of interventions aimed at prevention and treatment for this patient group.

scholarly journals Detection of Impending Aggressive Outbursts in Patients with Psychiatric Disorders: Violence Clues from Dogs

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Uriel Bakeman ◽  
Hodaya Eilam ◽  
Clara Moray Schild ◽  
Dan Grinstein ◽  
Yuval Eshed ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Medical Staff ◽  
Psychiatric Patients ◽  
Electronic Technology ◽  
Specific Patient ◽  
New Strategy ◽  
Response To Stress ◽  
Cortisol Levels

AbstractAggression in psychiatric wards is a continuing matter of concern for both patients and medical staff. Here we have tested the hypothesis that the frequency of such incidents can be reduced with a new strategy of using trained alert dogs that warn of impending violent outbursts. Dogs were positioned among patients in psychiatric wards. Analyses show that the dogs warned of impending aggressive outbursts, responding to signals from a specific patient out of a group of unfamiliar psychotic patients. Their alerts were not a response to stress as canine cortisol levels were not significantly changed. Visual glance was the preferred method used by young dogs to respond to patient. Until a similar electronic technology is developed, trained alert dogs can help caregivers to protect both the patient and those around them from injuries that may otherwise result from aggressive outbursts in psychiatric patients.

What's in a model? Network models as tools instead of representations of what psychiatric disorders really are

2019 ◽  
Vol 42 ◽  
Author(s):  
Hanna M. van Loo ◽  
Jan-Willem Romeijn
Keyword(s):  
Psychiatric Disorders ◽  
Network Models ◽  
Model Network

AbstractNetwork models block reductionism about psychiatric disorders only if models are interpreted in a realist manner – that is, taken to represent “what psychiatric disorders really are.” A flexible and more instrumentalist view of models is needed to improve our understanding of the heterogeneity and multifactorial character of psychiatric disorders.

Aerodynamic and Acoustic Voice Measures Before and After an Acute Public Speaking Stressor

2020 ◽  
Vol 63 (10) ◽  
pp. 3311-3325
Author(s):  
Brittany L. Perrine ◽  
Ronald C. Scherer
Keyword(s):  
Fundamental Frequency ◽  
Salivary Cortisol ◽  
Public Speaking ◽  
Stress System ◽  
Before And After ◽  
Subglottal Pressure ◽  
Response To Stress ◽  
System Activation ◽  
Speaking Fundamental Frequency ◽  
Pituitary Adrenal Axis

Purpose The goal of this study was to determine if differences in stress system activation lead to changes in speaking fundamental frequency, average oral airflow, and estimated subglottal pressure before and after an acute, psychosocial stressor. Method Eighteen vocally healthy adult females experienced the Trier Social Stress Test (TSST) to activate the hypothalamic–pituitary–adrenal axis. The TSST includes public speaking and performing mental arithmetic in front of an audience. At seven time points, three before the stressor and four after the stressor, the participants produced /pa/ repetitions, read the Rainbow Passage, and provided a saliva sample. Measures included (a) salivary cortisol level, (b) oral airflow, (c) estimated subglottal pressure, and (d) speaking fundamental frequency from the second sentence of the Rainbow Passage. Results Ten of the 18 participants experienced a hypothalamic–pituitary–adrenal axis response to stress as indicated by a 2.5-nmol/L increase in salivary cortisol from before the TSST to after the TSST. Those who experienced a response to stress had a significantly higher speaking fundamental frequency before and immediately after the stressor than later after the stressor. No other variable varied significantly due to the stressor. Conclusions This study suggests that the idiosyncratic and inconsistent voice changes reported in the literature may be explained by differences in stress system activation. In addition, laryngeal aerodynamic measures appear resilient to changes due to acute stress. Further work is needed to examine the influence of other stress systems and if these findings hold for dysphonic individuals.

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