scholarly journals Fear response-based prediction for stress susceptibility to PTSD-like phenotypes

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Min-Jae Jeong ◽  
Changhee Lee ◽  
Kibong Sung ◽  
Jung Hoon Jung ◽  
Jung Hyun Pyo ◽  
...  
Keyword(s):  
Analytical Approach ◽  
Intertrial Interval ◽  
Stress Disorder ◽  
Freezing Behavior ◽  
Fear Learning ◽  
Fear Response ◽  
Functional Implication ◽  
Behavioral Parameter ◽  
Underlying Mechanisms ◽  
Stress Susceptibility

Abstract Most individuals undergo traumatic stresses at some points in their life, but only a small proportion develop stress-related disorders such as anxiety diseases and posttraumatic stress disorder (PTSD). Although stress susceptibility is one determinant of mental disorders, the underlying mechanisms and functional implication remain unclear yet. We found that an increased amount of freezing that animals exhibited in the intertrial interval (ITI) of a stress-enhanced fear learning paradigm, predicts ensuing PTSD-like symptoms whereas resilient mice show ITI freezing comparable to that of unstressed mice. To examine the behavioral features, we developed a systematic analytical approach for ITI freezing and stress susceptibility. Thus, we provide a behavioral parameter for prognosis to stress susceptibility of individuals in the development of PTSD-like symptoms as well as a new mathematical means to scrutinize freezing behavior.

scholarly journals Fear response-based prediction for stress susceptibility to PTSD-like phenotypes

2020 ◽  
Author(s):  
Min-Jae Jeong ◽  
Changhee Lee ◽  
Ki-Bong Sung ◽  
Jung Hoon Jung ◽  
Jung-Hyun Pyo ◽  
...  
Keyword(s):  
Analytical Approach ◽  
Intertrial Interval ◽  
Stress Disorder ◽  
Freezing Behavior ◽  
Fear Learning ◽  
Fear Response ◽  
Functional Implication ◽  
Behavioral Parameter ◽  
Underlying Mechanisms ◽  
Stress Susceptibility

Abstract Most individuals undergo traumatic stresses at some points in their life, but only a small proportion develop stress-related disorders such as anxiety diseases and posttraumatic stress disorder (PTSD). Although stress susceptibility is one determinant of mental disorders, the underlying mechanisms and functional implication remain unclear yet. We found that an increased amount of freezing that animals exhibited in the intertrial interval (ITI) of a stress-enhanced fear learning paradigm, predicts ensuing PTSD-like symptoms whereas resilient mice show ITI freezing comparable to that of unstressed mice. To examine the behavioral features, we developed a systematic analytical approach for ITI freezing and stress susceptibility. Thus, we provide a behavioral parameter for prognosis to stress susceptibility of individuals in the development of PTSD-like symptoms as well as a new mathematical means to scrutinize freezing behavior.

scholarly journals Fear response-based prediction for stress susceptibility to PTSD-like phenotypes

2020 ◽  
Author(s):  
Min-Jae Jeong ◽  
Changhee Lee ◽  
Ki-Bong Sung ◽  
Jung Hoon Jung ◽  
Joung-Hun Kim
Keyword(s):  
Analytical Approach ◽  
Intertrial Interval ◽  
Stress Disorder ◽  
Freezing Behavior ◽  
Fear Learning ◽  
Fear Response ◽  
Functional Implication ◽  
Behavioral Parameter ◽  
Underlying Mechanisms ◽  
Stress Susceptibility

Abstract Most individuals undergo traumatic stresses at some points in their life, but only a small proportion develop stress-related disorders such as anxiety diseases and posttraumatic stress disorder (PTSD). Although stress susceptibility is one determinant of mental disorders, the underlying mechanisms and functional implication remain unclear yet. We found that an increased amount of freezing that animals exhibited in the intertrial interval (ITI) of a stress-enhanced fear learning paradigm, predicts ensuing PTSD-like symptoms whereas resilient mice show ITI freezing comparable to that of unstressed mice. To examine the behavioral features, we developed a systematic analytical approach for ITI freezing and stress susceptibility. Thus, we provide a behavioral parameter for prognosis to stress susceptibility of individuals in the development of PTSD-like symptoms as well as a new mathematical means to scrutinize freezing behavior.

scholarly journals Isoflurane Suppresses Stress-enhanced Fear Learning in a Rodent Model of Post–Traumatic Stress Disorder

2009 ◽  
Vol 110 (3) ◽  
pp. 487-495 ◽  
Author(s):  
Vinuta Rau ◽  
Irene Oh ◽  
Michael Laster ◽  
Edmond I. Eger ◽  
Michael S. Fanselow
Keyword(s):  
Nitrous Oxide ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Rodent Model ◽  
Fear Learning ◽  
Fear Response ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Inhaled Anesthetic

Background A minority of patients who experience awareness and/or pain during surgery subsequently develop post-traumatic stress disorder. In a rodent model of post-traumatic stress disorder, stress-enhanced fear learning (SEFL), rats are preexposed to a stressor of 15 foot shocks. Subsequent exposure to a single foot shock produces an enhanced fear response. This effect is akin to sensitized reactions shown by some post-traumatic stress disorder patients to cues previously associated with the traumatic event. Methods The authors studied the effect of isoflurane and nitrous oxide on SEFL. Rats were exposed to the inhaled anesthetic during or after a 15-foot shock stressor. Then, rats were given a single foot shock in a different environment. Their fear response was quantified in response to the 15-foot shock and single-foot shock environments. SEFL longevity was tested by placing a 90-day period between the 15 foot shocks and the single foot shock. In addition, the intensity of the foot shock was increased to evaluate treatment effectiveness. Results Increasing isoflurane concentrations decreased SEFL when given during, but not after, the stressor. At 0.40 minimum alveolar concentration (MAC), isoflurane given during the stressor blocked SEFL 90 days later. A threefold increase in the stressor intensity increased the isoflurane concentration required to block SEFL to no more than 0.67 MAC. As with isoflurane, nitrous oxide suppressed SEFL at a similar MAC fraction. Conclusions These results suggest that sufficient concentrations (perhaps 0.67 MAC or less) of an inhaled anesthetic may prevent SEFL.

scholarly journals Dissociable control of unconditioned responses and associative fear learning by parabrachial CGRP neurons

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Anna J Bowen ◽  
Jane Y Chen ◽  
Y Waterlily Huang ◽  
Nathan A Baertsch ◽  
Sekun Park ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Behavioral Responses ◽  
Freezing Behavior ◽  
Fear Learning ◽  
Autonomic Arousal ◽  
Flexible Control ◽  
Somatic Pain ◽  
Unpredictable Environments ◽  
Adaptive Processes ◽  
Simultaneous Activation

Parabrachial CGRP neurons receive diverse threat-related signals and contribute to multiple phases of adaptive threat responses in mice, with their inactivation attenuating both unconditioned behavioral responses to somatic pain and fear-memory formation. Because CGRPPBN neurons respond broadly to multi-modal threats, it remains unknown how these distinct adaptive processes are individually engaged. We show that while three partially separable subsets of CGRPPBN neurons broadly collateralize to their respective downstream partners, individual projections accomplish distinct functions: hypothalamic and extended amygdalar projections elicit assorted unconditioned threat responses including autonomic arousal, anxiety, and freezing behavior, while thalamic and basal forebrain projections generate freezing behavior and, unexpectedly, contribute to associative fear learning. Moreover, the unconditioned responses generated by individual projections are complementary, with simultaneous activation of multiple sites driving profound freezing behavior and bradycardia that are not elicited by any individual projection. This semi-parallel, scalable connectivity schema likely contributes to flexible control of threat responses in unpredictable environments.

scholarly journals Amygdala Transcriptome and Cellular Mechanisms Underlying Stress-Enhanced Fear Learning in a Rat Model of Posttraumatic Stress Disorder

2010 ◽  
Vol 35 (6) ◽  
pp. 1402-1411 ◽  
Author(s):  
Igor Ponomarev ◽  
Vinuta Rau ◽  
Edmond I Eger ◽  
R Adron Harris ◽  
Michael S Fanselow
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Rat Model ◽  
Stress Disorder ◽  
Fear Learning ◽  
Cellular Mechanisms

scholarly journals Oxytocin receptor activation does not mediate associative fear deficits in a Williams Syndrome model

2021 ◽  
Author(s):  
Kayla R. Nygaard ◽  
Raylynn G. Swift ◽  
Rebecca M. Glick ◽  
Rachael E. Wagner ◽  
Susan E. Maloney ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Williams Syndrome ◽  
Conditioned Fear ◽  
Fear Memory ◽  
Receptor Activation ◽  
Oxytocin Receptor ◽  
Receptor Expression ◽  
Fear Learning ◽  
Underlying Mechanisms ◽  
Complete Deletion

ABSTRACTWilliams Syndrome is caused by a deletion of 26-28 genes on chromosome 7q11.23. Patients with this disorder have distinct behavioral phenotypes including learning deficits, anxiety, increased phobias, and hypersociability. Some studies also suggest elevated blood oxytocin and altered oxytocin receptor expression, and this oxytocin dysregulation is hypothesized to be involved in the underlying mechanisms driving a subset of these phenotypes. A ‘Complete Deletion’ mouse, modeling the hemizygous critical region deletion in Williams Syndrome, recapitulates many of the phenotypes present in humans. These Complete Deletion mice also exhibited impaired fear responses in the conditioned fear task. Here, we address whether oxytocin dysregulation is responsible for this impaired associative fear memory response. We show direct delivery of an oxytocin receptor antagonist to the central nervous system did not rescue the attenuated contextual or cued fear memory responses in Complete Deletion mice. Thus, increased oxytocin signaling is not acutely responsible for this phenotype. We also evaluated oxytocin receptor and serotonin transporter availability in regions related to fear learning, memory, and sociability using autoradiography in wild type and Complete Deletion mice. While we identified trends in lowered oxytocin receptor expression in the lateral septal nucleus, and trends towards lowered serotonin transporter availability in the striatum and orbitofrontal cortex, we found no significant differences after correction. Together, these data suggest the fear conditioning anomalies in the Williams Syndrome mouse model are independent of any alterations in the oxytocinergic system caused by deletion of the Williams locus.

Antidepressants in Post-Traumatic Stress Disorder

2018 ◽  
Author(s):  
N. Koen ◽  
T. Amos ◽  
J. Ipser ◽  
D. Stein
Keyword(s):  
Traumatic Stress ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Tricyclic Antidepressants ◽  
Stress Disorder ◽  
Antidepressant Treatment ◽  
Post Traumatic Stress ◽  
Psychotropic Agents ◽  
Antidepressant Efficacy ◽  
Post Traumatic ◽  
Underlying Mechanisms

This chapter discusses the use of antidepressants in treating symptoms of posttraumatic stress disorder (PTSD). Tricyclic antidepressants were the first psychotropic agents to be studied systematically and rigorously for the treatment of PTSD. While early studies focused both on the tricyclics and monoamine oxidase inhibitors (MAOIs), more recent work has centered on the selective serotonin reuptake inhibitors (SSRIs); and paroxetine and sertraline are currently approved by the U.S. Food and Drug Administration (FDA) for use in this disorder. However, given the relatively small effect sizes in SSRI trials of PTSD, there is a need for ongoing psychopharmacological research to understand underlying mechanisms of antidepressant efficacy and to optimize response to pharmacotherapy. Further data on pediatric PTSD and on medication prophylaxis are needed before routine antidepressant treatment can be endorsed in these contexts.

scholarly journals Exposure Therapy for Post-Traumatic Stress Disorder: Factors of Limited Success and Possible Alternative Treatment

2020 ◽  
Vol 10 (3) ◽  
pp. 167 ◽  
Author(s):  
Sara Markowitz ◽  
Michael Fanselow
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Exposure Therapy ◽  
Fear Response ◽  
Post Traumatic Stress ◽  
Limited Success ◽  
Amygdala Activity ◽  
Post Traumatic

Recent research indicates that there is mixed success in using exposure therapies on patients with post-traumatic stress disorder (PTSD). Our study argues that there are two major reasons for this: The first is that there are nonassociative aspects of PTSD, such as hyperactive amygdala activity, that cannot be attenuated using the exposure therapy; The second is that exposure therapy is conceptualized from the theoretical framework of Pavlovian fear extinction, which we know is heavily context dependent. Thus, reducing fear response in a therapist’s office does not guarantee reduced response in other situations. This study also discusses work relating to the role of the hippocampus in context encoding, and how these findings can be beneficial for improving exposure therapies.

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