Special Issue "From Synapses to Syndromes in Stress Research: Translational Approaches to the Study of the Neurobiology of Stress-Related Mental Disorders"

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A special issue of Behavioral Sciences (ISSN 2076-328X).

Deadline for manuscript submissions: closed (31 March 2012)

Special Issue Editor

Guest Editor
Prof. Dr. David Diamond

1 Departments of Psychology, Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD, USF Neuroscience Collaborative, University of South Florida, 4202 East Fowler Ave., Tampa, Florida 33620, USA
2 Research and Development Service, J.A. Haley Veterans Hospital, 13000 Bruce B. Downs Blvd., Tampa, FL 33612, USA
Website | E-Mail
Phone: +1 813 974 0480
Fax: +1 813 974 4617
Interests: stress; fear; memory; hippocampus; amygdala; frontal cortex; synaptic plasticity; long-term potentiation

Special Issue Information

Dear Colleagues,

Fear and stress-provoking experiences generate changes in the brain and behavior that can last from minutes to a lifetime. An experience-induced increase in arousal can have a constructive outcome, producing an enhancement of memory for important events and an improvement in behavioral performance. However, intense fear-provoking experiences can generate pathological outcomes. Traumatic stress contributes to the development of debilitating mood and anxiety disorders, including depression and post-traumatic stress disorder, and has been associated with a broad range of mental and neurodegenerative disorders, including Alzheimer’s disease, phobias, schizophrenia and multiple sclerosis. This special issue of Behavioral Sciences targets a broad range of research addressing the effects of stress on brain, behavior and mental disease at mechanistic, preclinical and clinical levels of analysis.

Prof. Dr. David Diamond
Guest Editor

Published Papers (6 papers)

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Research

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Open AccessArticle Brief Treatment of Symptoms of Post-Traumatic Stress Disorder (PTSD) by Use of Accelerated Resolution Therapy (ART®)
Behav. Sci. 2012, 2(2), 115-134; doi:10.3390/bs2020115
Received: 27 April 2012 / Revised: 6 June 2012 / Accepted: 12 June 2012 / Published: 18 June 2012
Cited by 5 | PDF Full-text (308 KB) | HTML Full-text | XML Full-text
Abstract
Post-Traumatic Stress Disorder (PTSD) is a prevalent, disabling anxiety disorder. This prospective cohort study reports on a new exposure-based therapy known as Accelerated Resolution Therapy (ART®) that incorporates the use of eye movements administered in a brief treatment period (1–5 one-hour
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Post-Traumatic Stress Disorder (PTSD) is a prevalent, disabling anxiety disorder. This prospective cohort study reports on a new exposure-based therapy known as Accelerated Resolution Therapy (ART®) that incorporates the use of eye movements administered in a brief treatment period (1–5 one-hour sessions within three weeks). Eighty adults aged 21–60 years with symptoms of PTSD were recruited from the Tampa Bay area. The ART-based psychotherapy was designed to minimize anxiety and body sensations associated with recall of traumatic memories and to replace distressing images with favorable ones. Participants’ mean age was 40 years, 77% were female, and 29% were Hispanic. Participants underwent a median of three ART sessions, 66 of 80 (82.5%) completed treatment, and 54 of 66 (81.8%) provided 2-month follow-up data. Mean scores pre- and post-ART and at 2-month follow-up were: PTSD Checklist: 54.5 ± 12.2 vs. 31.2 ± 11.4 vs. 30.0 ± 12.4; Brief Symptom Inventory: 30.8 ± 14.6 vs. 10.1 ± 10.8 vs. 10.1 ± 12.1; Center for Epidemiologic Studies Depression Scale: 29.5 ± 10.9 vs. 11.8 ± 11.1 vs. 13.5 ± 12.1; Trauma Related Growth Inventory-Distress scale: 18.9 ± 4.1 vs. 7.4 ± 5.9 vs. 8.2 ± 5.9 (p < 0.0001 for all pre-ART vs. post-ART and 2-month comparisons). No serious adverse events were reported. ART appears to be a brief, safe, and effective treatment for symptoms of PTSD. Full article
Open AccessArticle Symptom Persistence and Memory Performance in Posttraumatic Stress Disorder: A Gene X Environment Pilot Study
Behav. Sci. 2012, 2(2), 103-114; doi:10.3390/bs2020103
Received: 25 April 2012 / Revised: 24 May 2012 / Accepted: 24 May 2012 / Published: 1 June 2012
Cited by 1 | PDF Full-text (193 KB) | HTML Full-text | XML Full-text
Abstract
The FKBP5 gene, a glucocorticoid receptor (GR)-regulating co-chaperone of stress proteins, is of special interest because of its role in hypothalamic-pituitary-adrenal (HPA)-axis regulation. However, studies finding a genetic relationship between posttraumatic stress disorder (PTSD) and the FKBP5 gene have failed to distinguish between
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The FKBP5 gene, a glucocorticoid receptor (GR)-regulating co-chaperone of stress proteins, is of special interest because of its role in hypothalamic-pituitary-adrenal (HPA)-axis regulation. However, studies finding a genetic relationship between posttraumatic stress disorder (PTSD) and the FKBP5 gene have failed to distinguish between the development and persistence of PTSD, thereby limiting the prognostic usefulness of such a finding. The present study sought to longitudinally explore this question by examining the association between four single-nucleotide polymorphisms (SNPs) in the FKBP5 gene (rs3800373, rs9470080, rs1360780, and rs9296158), the persistence of PTSD (severity and diagnostic status), and memory performance among twenty-two treatment-seekers diagnosed with acute PTSD. Results showed that the four SNPs significantly interacted with improvement in PTSD symptoms as well as PTSD diagnostic status. Individuals homozygous for the dominant allele and having experienced higher levels of peritraumatic responses subsequently showed more memory dysfunction. The results of this study suggest that SNPs in the FKBP5 gene are associated with symptom persistence and memory dysfunction in acute PTSD. Full article
Open AccessArticle Physiological Consequences of Repeated Exposures to Conditioned Fear
Behav. Sci. 2012, 2(2), 57-78; doi:10.3390/bs2020057
Received: 5 April 2012 / Revised: 5 May 2012 / Accepted: 14 May 2012 / Published: 18 May 2012
Cited by 6 | PDF Full-text (1932 KB) | HTML Full-text | XML Full-text
Abstract
Activation of the stress response evokes a cascade of physiological reactions that may be detrimental when repeated or chronic, and when triggered after exposure to psychological/emotional stressors. Investigation of the physiological mechanisms responsible for the health damaging effects requires animal paradigms that repeatedly
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Activation of the stress response evokes a cascade of physiological reactions that may be detrimental when repeated or chronic, and when triggered after exposure to psychological/emotional stressors. Investigation of the physiological mechanisms responsible for the health damaging effects requires animal paradigms that repeatedly evoke a response to psychological/emotional stressors. To this end, adult male Sprague Dawley rats were repeatedly exposed (2X per day for 20 days) to a context that they were conditioned to fear (conditioned fear test, CFT). Repeated exposure to CFT produced body weight loss, adrenal hypertrophy, thymic involution, and basal corticosterone elevation. In vivo biotelemetry measures revealed that CFT evokes sympathetic nervous system driven increases in heart rate (HR), mean arterial pressure (MAP), and core body temperature. Extinction of behavioral (freezing) and physiological responses to CFT was prevented using minimal reinstatement footshock. MAP responses to the CFT did not diminish across 20 days of exposure. In contrast, HR and cardiac contractility responses declined by day 15, suggesting a shift toward vascular-dominated MAP (a pre-clinical marker of CV dysfunction). Flattened diurnal rhythms, common to stress-related mood/anxiety disorders, were found for most physiological measures. Thus, repeated CFT produces adaptations indicative of the health damaging effects of psychological/emotional stress. Full article
Open AccessArticle Stress Alters the Discriminative Stimulus and Response Rate Effects of Cocaine Differentially in Lewis and Fischer Inbred Rats
Behav. Sci. 2012, 2(1), 23-37; doi:10.3390/bs2010023
Received: 19 January 2012 / Revised: 9 February 2012 / Accepted: 17 February 2012 / Published: 1 March 2012
Cited by 1 | PDF Full-text (367 KB) | HTML Full-text | XML Full-text
Abstract
Stress enhances the behavioral effects of cocaine, perhaps via hypothalamic-pituitary-adrenal (HPA) axis activity. Yet, compared to Fischer 344 (F344) rats, Lewis rats have hyporesponsive HPA axis function and more readily acquire cocaine self-administration. We hypothesized that stress would differentially affect cocaine behaviors in
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Stress enhances the behavioral effects of cocaine, perhaps via hypothalamic-pituitary-adrenal (HPA) axis activity. Yet, compared to Fischer 344 (F344) rats, Lewis rats have hyporesponsive HPA axis function and more readily acquire cocaine self-administration. We hypothesized that stress would differentially affect cocaine behaviors in these strains. The effects of three stressors on the discriminative stimulus and response rate effects of cocaine were investigated. Rats of both strains were trained to discriminate cocaine (10 mg/kg) from saline using a two-lever, food-reinforced (FR10) procedure. Immediately prior to cumulative dose (1, 3, 10 mg/kg cocaine) test sessions, rats were restrained for 15-min, had 15-min of footshock in a distinct context, or were placed in the shock-paired context. Another set of F344 and Lewis rats were tested similarly except they received vehicle injections to test if stress substituted for cocaine. Most vehicle-tested rats failed to respond after stressor exposures. Among cocaine-tested rats, restraint stress enhanced cocaine’s discriminative stimulus effects in F344 rats. Shock and shock-context increased response rates in Lewis rats. Stress-induced increases in corticosterone levels showed strain differences but did not correlate with behavior. These data suggest that the behavioral effects of cocaine can be differentially affected by stress in a strain-selective manner. Full article

Review

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Open AccessReview Behavioral Studies and Genetic Alterations in Corticotropin-Releasing Hormone (CRH) Neurocircuitry: Insights into Human Psychiatric Disorders
Behav. Sci. 2012, 2(2), 135-171; doi:10.3390/bs2020135
Received: 15 April 2012 / Revised: 23 May 2012 / Accepted: 15 June 2012 / Published: 21 June 2012
Cited by 13 | PDF Full-text (360 KB) | HTML Full-text | XML Full-text
Abstract
To maintain well-being, all organisms require the ability to re-establish homeostasis in the presence of adverse physiological or psychological experiences. The regulation of the hypothalamic-pituitary adrenal (HPA) axis during stress is important in preventing maladaptive responses that may increase susceptibility to affective disorders.
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To maintain well-being, all organisms require the ability to re-establish homeostasis in the presence of adverse physiological or psychological experiences. The regulation of the hypothalamic-pituitary adrenal (HPA) axis during stress is important in preventing maladaptive responses that may increase susceptibility to affective disorders. Corticotropin-releasing hormone (CRH) is a central stress hormone in the HPA axis pathway and has been implicated in stress-induced psychiatric disorders, reproductive and cardiac function, as well as energy metabolism. In the context of psychiatric disorders, CRH dysfunction is associated with the occurrence of post-traumatic stress disorder, major depression, anorexia nervosa, and anxiety disorders. Here, we review the synthesis, molecular signaling and regulation, as well as synaptic activity of CRH. We go on to summarize studies of altered CRH signaling in mutant animal models. This assembled data demonstrate an important role for CRH in neuroendocrine, autonomic, and behavioral correlates of adaptation and maladaptation. Next, we present findings regarding human genetic polymorphisms in CRH pathway genes that are associated with stress and psychiatric disorders. Finally, we discuss a role for regulators of CRH activity as potential sites for therapeutic intervention aimed at treating maladaptive behaviors associated with stress. Full article
Open AccessReview Developmental Neurobiology of the Rat Attachment System and Its Modulation by Stress
Behav. Sci. 2012, 2(2), 79-102; doi:10.3390/bs2020079
Received: 31 March 2012 / Revised: 8 May 2012 / Accepted: 10 May 2012 / Published: 18 May 2012
Cited by 2 | PDF Full-text (350 KB) | HTML Full-text | XML Full-text
Abstract
Stress is a powerful modulator of brain structure and function. While stress is beneficial for survival, inappropriate stress dramatically increases the risk of physical and mental health problems, particularly when experienced during early developmental periods. Here we focus on the neurobiology of the
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Stress is a powerful modulator of brain structure and function. While stress is beneficial for survival, inappropriate stress dramatically increases the risk of physical and mental health problems, particularly when experienced during early developmental periods. Here we focus on the neurobiology of the infant rat’s odor learning system that enables neonates to learn and approach the maternal odor and describe the unique role of the stress hormone corticosterone in modulating this odor approach learning across development. During the first nine postnatal days, this odor approach learning of infant rats is supported by a wide range of sensory stimuli and ensures attachment to the mother’s odor, even when interactions with her are occasionally associated with pain. With maturation and the emergence of a stress- or pain-induced corticosterone response, this odor approach learning terminates and a more adult-like amygdala-dependent fear/avoidance learning emerges. Strikingly, the odor approach and attenuated fear learning of older pups can be re-established by the presence of the mother, due to her ability to suppress her pups’ corticosterone release and amygdala activity. This suggests that developmental changes in stress responsiveness and the stimuli that produce a stress response might be critically involved in optimally adapting the pup’s attachment system to its respective ecological niche. Full article
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