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      Early Life Trauma and Attachment: Immediate and Enduring Effects on Neurobehavioral and Stress Axis Development

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          Abstract

          Over half a century of converging clinical and animal research indicates that early life experiences induce enduring neuroplasticity of the HPA-axis and the developing brain. This experience-induced neuroplasticity is due to alterations in the frequency and intensity of stimulation of pups’ sensory systems (i.e., olfactory, somatosensory, gustatory) embedded in mother–infant interactions. This stimulation provides “hidden regulators” of pups’ behavioral, physiological, and neural responses that have both immediate and enduring consequences, including those involving the stress response. While variation in stimulation can produce individual differences and adaptive behaviors, pathological early life experiences can induce maladaptive behaviors, initiate a pathway to pathology, and increase risk for later-life psychopathologies, such as mood and affective disorders, suggesting that infant-attachment relationships program later-life neurobehavioral function. Recent evidence suggests that the effects of maternal presence or absence during this sensory stimulation provide a major modulatory role in neural and endocrine system responses, which have minimal impact on pups’ immediate neurobehavior but a robust impact on neurobehavioral development. This concept is reviewed here using two complementary rodent models of infant trauma within attachment: infant paired-odor-shock conditioning (mimicking maternal odor attachment learning) and rearing with an abusive mother that converge in producing a similar behavioral phenotype in later-life including depressive-like behavior as well as disrupted HPA-axis and amygdala function. The importance of maternal social presence on pups’ immediate and enduring brain and behavior suggests unique processing of sensory stimuli in early life that could provide insight into the development of novel strategies for prevention and therapeutic interventions for trauma experienced with the abusive caregiver.

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          Depression: a new animal model sensitive to antidepressant treatments.

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            How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions

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              The link between childhood trauma and depression: insights from HPA axis studies in humans.

              Childhood trauma is a potent risk factor for developing depression in adulthood, particularly in response to additional stress. We here summarize results from a series of clinical studies suggesting that childhood trauma in humans is associated with sensitization of the neuroendocrine stress response, glucocorticoid resistance, increased central corticotropin-releasing factor (CRF) activity, immune activation, and reduced hippocampal volume, closely paralleling several of the neuroendocrine features of depression. Neuroendocrine changes secondary to early-life stress likely reflect risk to develop depression in response to stress, potentially due to failure of a connected neural circuitry implicated in emotional, neuroendocrine and autonomic control to compensate in response to challenge. However, not all of depression is related to childhood trauma and our results suggest the existence of biologically distinguishable subtypes of depression as a function of childhood trauma that are also responsive to differential treatment. Other risk factors, such as female gender and genetic dispositions, interfere with components of the stress response and further increase vulnerability for depression. Similar associations apply to a spectrum of other psychiatric and medical disorders that frequently coincide with depression and are aggravated by stress. Taken together, this line of evidence demonstrates that psychoneuroendocrine research may ultimately promote optimized clinical care and help prevent the adverse outcomes of childhood trauma.
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                Author and article information

                Contributors
                URI : http://frontiersin.org/people/u/101593
                URI : http://frontiersin.org/people/u/2553
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                08 February 2014
                21 March 2014
                2014
                : 5
                : 33
                Affiliations
                [1] 1Department of Neuroscience and Physiology, Sackler Institute for Graduate Biomedical Sciences, New York University School of Medicine , New York, NY, USA
                [2] 2Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research , New York, NY, USA
                [3] 3New York University Child Study Center, Department of Child and Adolescent Psychiatry, New York University School of Medicine , New York, NY, USA
                Author notes

                Edited by: Nikolaos P. Daskalakis, Icahn School of Medicine at Mount Sinai, USA

                Reviewed by: Aniko Korosi, University of Amsterdam, Netherlands; James A. Carr, Texas Tech University, USA

                *Correspondence: Millie Rincón-Cortés, Sullivan Laboratory, New York University Child Study Center, Department of Child and Adolescent Psychiatry, New York University School of Medicine, 1 Park Avenue, New York, NY 10016, USA e-mail: millie.rinconcortes@ 123456med.nyu.edu

                This article was submitted to Neuroendocrine Science, a section of the journal Frontiers in Endocrinology.

                Article
                10.3389/fendo.2014.00033
                3968754
                24711804
                c24fbe68-e8a0-440f-a516-0a10827e4774
                Copyright © 2014 Rincón-Cortés and Sullivan.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 15 December 2013
                : 05 March 2014
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 346, Pages: 15, Words: 14696
                Categories
                Endocrinology
                Review Article

                Endocrinology & Diabetes
                infant-attachment,maternal programming,development,amygdala,social behavior,rodent models,stress

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