LDH ASSESSMENT OF DIFFERENTIAL EARLY STRESS IN RATS.

This chapter provides a review of research and a description of the central issues regarding the stressor of depression in mothers during pregnancy and the postpartum periods in relation to risk for the development of psychopathology in offspring. Where evidence allows, causal relations are emphasized; otherwise, limitations are noted, especially those regarding being able to draw causal conclusions from the correlational approaches typically taken in this area of study. Evidence for mechanisms in the transmission of risk is also described, given the potential for understanding causal relations. With the developmental psychopathology perspective of depression as a stressor for offspring, the focus is on vulnerabilities to and early signs of disorder as well as mental health outcomes per se. The chapter concludes with suggested critical issues in the field and recommendations for future directions for research.

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The Effect of Nutrition on Early Stress-Induced Hyperglycemia, Serum Insulin Levels, and Exogenous Insulin Administration in Critically Ill Patients With Septic Shock

Shock ◽

10.1097/shk.0000000000001287 ◽

2019 ◽

Vol 52 (4) ◽

pp. e31-e38 ◽

Cited By ~ 1

Author(s):

Nikki Treskes ◽

Wilhelmina Aria Christina Koekkoek ◽

Arthur Raymond Hubert van Zanten

Keyword(s):

Septic Shock ◽

Critically Ill ◽

Critically Ill Patients ◽

Serum Insulin ◽

Exogenous Insulin ◽

Insulin Administration ◽

Insulin Levels ◽

Early Stress

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Association of Early Stress Testing with Outcomes for Emergency Department Evaluation of Suspected Acute Coronary Syndrome

Critical Pathways in Cardiology ◽

10.1097/hpc.0000000000000068 ◽

2016 ◽

Vol 15 (2) ◽

pp. 60-68 ◽

Cited By ~ 4

Author(s):

Benjamin C. Sun ◽

Amber Laurie ◽

Rongwei Fu ◽

Maros Ferencik ◽

Michael Shapiro ◽

...

Keyword(s):

Emergency Department ◽

Acute Coronary Syndrome ◽

Stress Testing ◽

Coronary Syndrome ◽

Early Stress ◽

Department Evaluation

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Why are there lasting effects from exposure to stress during development? An analysis of current models of early stress

Physiology & Behavior ◽

10.1016/j.physbeh.2016.05.032 ◽

2016 ◽

Vol 164 ◽

pp. 164-181 ◽

Cited By ~ 13

Author(s):

Lauren E. Chaby

Keyword(s):

Early Stress

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Connect-the-DOT from early stress to depression

Science Signaling ◽

10.1126/scisignal.abi9138 ◽

2021 ◽

Vol 14 (678) ◽

pp. eabi9138

Author(s):

Leslie K. Ferrarelli

Keyword(s):

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Behavioral Effects ◽

Early Stress

Targeting the epigenetic enzyme DOT1L may reverse some behavioral effects of early-life stress.

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Central role of the habenulo-interpeduncular system in the neurodevelopmental basis of susceptibility and resilience to anxiety

10.21203/rs.3.rs-823079/v1 ◽

2021 ◽

Author(s):

Malalaniaina Rakotobe ◽

Niels Fjerdingstad ◽

Nuria Ruiz-Reig ◽

Thomas Lamonerie ◽

Fabien D'Autréaux

Keyword(s):

Stress Response ◽

Brain Development ◽

Chronic Stress ◽

Environmental Stressors ◽

Critical Node ◽

Sensitive Periods ◽

Early Stress ◽

Effects Of Stress

Abstract Experiencing stress during sensitive periods of brain development has a major impact on how individuals cope with later stress. Although many become more prone to develop anxiety or depression, some appear resilient. The mechanisms underlying these differences are unknown. Key answers may lie in how genetic and environmental stressors interact to shape the circuits controlling emotions. Here we studied the role of the habenulo-interpeducuncular system (HIPS), a critical node of reward circuits, in early stress-induced anxiety. We found that a subcircuit of this system, characterized by Otx2 expression, is particularly responsive to chronic stress during puberty, which induces HIPS hypersensitivity to later stress and susceptibility to develop anxiety. We further show that Otx2 deletion restricted to the HIPS counteracts these effects of stress. Together, these results demonstrate that Otx2 and stress interact, around puberty, to shape the HIPS stress-response, revealed here as a key modulator of susceptibility/resilience to develop anxiety.

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