DOCSLIB.ORG

Effect of Chronic Stress Exposure on Beta-Adrenergic Receptor Signaling and Fear- Learning

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Effect of Chronic Stress Exposure on Beta-adrenergic Receptor Signaling and Fear- Learning A dissertation submitted to Kent State University in partial fulfillment of the requirements for the degree of Doctor of Philosophy By Robert Michael Camp June 2015 © Copyright All rights reserved Except for previously published materials Dissertation written by Robert M. Camp B.A. Kent State University, 2009 Ph.D. Kent State University, 2015 Approved by __________________________________________________ Dr. John D. Johnson, Advisor, Department of Biological Sciences __________________________________________________ Dr. Eric M. Mintz, Member, Department of Biological Sciences __________________________________________________ Dr. Heather K. Caldwell, Member, Department of Biological Sciences __________________________________________________ Dr. Aaron M. Jasnow, Outside member, Department of Psychology __________________________________________________ Dr. David C. Riccio, Graduate faculty representative, Department of Psychology Accepted by __________________________________________________ Dr. Laura G. Leff, Chair, Department of Biological Sciences __________________________________________________ Dr. James L. Blank, Dean, College of Arts & Sciences ii Table of Contents Page List of Figures………………………………………………………………………………….viii List of Abbreviations…………………………………………………………………………….x Acknowledgements…………………………………………………………………………….xii Chapter I. Introduction………………………………………………………………………….1 Stress, defined…………………………………………………………………………..1 Stress and psychological disorder…………………………………………………….2 Selye and the GAS, Cannon and “Fight-or-Flight”.................................................5 The neuroendocrine stress response………………………………………………...7 The central stress response………………………………………………………….11 Memory, stress, and norepinephrine………………………………………………...14 Repeated stress alters noradrenergic signaling……………………………………16 Focus of dissertation…………………………………………………………………..17 Chapter II. Strain- and context-dependent effects of repeated stressor exposure on the expression of depressive-like behavior in rats……………………………………………..22 Introduction…………………………………………………………………………….22 Methods and procedures……………………………………………………………..25 Subjects..……………………………………………………………………….25 Drug delivery…………………………………………………………………...26 Repeated stress protocol……………………………………………………..27 Sucrose preference measurements………………………………………....28 iii Behavioral measurements…………………………………………………....28 Organ weight and stress hormone measurement………………………….29 Statistical analysis……………………………………………………………..30 Study 1: effects of context on behavioral changes in animals exposed to chronic stress……………………………………………………………….….30 Study 2: the role of β-ARs in enhanced contextual fear conditioning in chronically stressed animals………………………………………………....30 Study 3: differential effects of chronic stress between central and peripheral β-ARs……………………………………………………………....31 Study 4: disparity between laboratory rat strains in effects of chronic mild stress exposure..………………………………………………………………31 Results………………………………………………………………………………….32 Study 1: effect of context on repeated stress-induced behavioral changes………………………………………………………………………...32 Study 2: effect of propranolol on repeated stress-induced behavioral changes………………………………………………………………………...37 Study 2: effect of propranolol on stress-induced changes in body and organ weights..………………………………………………………………...43 Study 2: effect of propranolol on corticosterone levels following acute and repeated stressor exposure………………………………………………….46 Study 3: effect of nadolol on repeated stress-induced behavioral changes………………………………………………………………………...49 iv Study 3: effect of nadolol on spleen weight following repeated stressor exposure…...…………………………………………………………………...54 Study 4: effects of repeated stress-induced behavioral changes in Sprague-Dawley rats….……………………………………………………….54 Discussion………………………………………………………………………………58 Conclusion……………………………………………………………………………...62 Chapter III: Repeated stressor exposure enhances contextual fear memory in a beta- adrenergic receptor-dependent process and increases impulsivity in a non-beta receptor-dependent fashion...………………………………………………………………...64 Introduction……………………………………………………………………………..64 Methods and materials…….…………………………………………………………..66 Subjects…………………………………………………………………………66 Repeated stress protocol……………………………………………………...67 Behavioral testing………………………………………………………………68 Conditioned fear………………………………………………………..68 Open field...……………………………………………………………..69 Passive avoidance….………………………………………………….69 Beta-adrenergic receptor antagonist administration……………………….70 Statistical analysis……………………………………………………………..70 Experimental design…………………………………………………………..70 Results………………………………………………………………………………….71 Effect of CMS on freezing behavior………………………………………….71 v Effect of CMS on passive avoidance behavior……………………………..74 Effect of repeated stress on non-contextual anxiety-like behavior……….74 Discussion……………………………………………………………………………...76 Chapter IV: Effects of chronic mild stress on sensitization of beta-adrenergic receptor- stimulated intracellular signaling in amygdaloid and hippocampal tissue……………….80 Introduction……………………………………………………………………………..80 Methods and procedures……………………………………………………………...83 Subjects…………………………………………………………………………83 Chronic mild stress protocol……...…………………………………………...83 Beta-adrenergic receptor stimulation………………………………………...83 Cellular signaling analysis…………………………………………………….84 Statistical analysis……………………………………………………………..84 Experimental design………………………………………………….………..85 Results……………………………………………………………………….………….85 Effect of stress and propranolol on intracellular signaling in the amygdala……………………………………………………………………….85 Effect of propranolol on intracellular signaling on intracellular signaling in the hippocampus……………………………………………………………….89 Discussion………………………………………………………………………………92 Chapter V: Global discussion………………………………………………………………...95 Future directions……………………………………………………………………...103 Final thoughts…………………………………………………………………………105 vi References……………………………………………………………………………………107 vii List of figures Page Chapter I. Introduction Fig. 1. The HPA axis and the sympathetic nervous system………………………………..8 Fig. 2. Hypothetical process of stress-induced enhancement of fear memory…………18 Fig. 3. Intracellular signaling at β-ARs………………………………………………………21 Chapter II. Strain- and context-dependent effects of repeated stressor exposure on the expression of depressive-like behavior in rats Fig. 4. Effects of context on behaviors following repeated stressor exposure………….33 Fig. 5. Effects of chronic propranolol infusion on behaviors following repeated stressor exposure………………………………………………………………………………………..38 Fig. 6. Effects of chronic propranolol infusion and repeated stressor exposure on body and organ weights……………………………………………………………………………..44 Fig. 7. Effects of chronic propranolol infusion on corticosterone responses…………….47 Fig. 8. Effects of chronic nadolol infusion on behaviors following repeated stressor exposure………………………………………………………………………………………..50 Fig. 9. Effect of chronic nadolol infusion and repeated stressor exposure on spleen weight…………………………………………………………………………………………...55 Fig. 10. Behavioral effects of repeated stressor exposure in Sprague-Dawley rats.…..56 Chapter III: Repeated stressor exposure enhances contextual fear memory in a beta- adrenergic receptor-dependent process and increases impulsivity in a non-beta viii receptor-dependent fashion Fig. 11. Effects of chronic mild stress on contextual fear conditioning…………………..72 Fig. 12. Effects of chronic mild stress on latency in a passive avoidance test..….……..73 Fig. 13. Effects of chronic mild stress on open field behavior.……………………………75 Chapter IV. Effects of chronic mild stress on sensitization of beta-adrenergic receptor- stimulated intracellular signaling in amygdaloid and hippocampal tissue Fig. 14. Effects on intracellular signaling in the amygdala following repeated stressor exposure………………………………………………………………………………………..86 Fig. 15. Effects on intracellular signaling in the hippocampus following repeated stressor exposure………………………………………………………………………………………..90 Chapter V. Global discussion Fig. 16. Observed process of stress-induced enhancement of fear memory...…………96 Fig. 17. Additional components of signaling at β-ARs……………………………………102 ix List of abbreviations ACTH - adrenocorticotropic hormone AMPA(R) - α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (receptor) β-AR - beta-adrenergic receptor BDNF - brain-derived neurotrophic factor BLA - basolateral nucleus of the amygdala CAMK-IV - calmodulin kinase IV cAMP - 3’-5’-cyclic adenosine monophosphate CMS - chronic mild stress CORT - corticosterone or cortisol CREB - cAMP response element-binding CRH - corticotropin-releasing hormone DEX - dexamethasone EDTA - ethylenediaminetetraacetic acid ELISA - enzyme-linked immunosorbent assay ERK - extracellular signal-regulated kinase GAD - generalized anxiety disorder GAS - general adaptation syndrome GR – glucocorticoid receptor GluR1 - glutamate receptor 1 HCC – home cage controls HPA - hypothalamic-pituitary-adrenal x IL-1β - interleukin-1 beta IL-6 - interleukin-6 LC - locus cœruleus LTP - long-term potentiation MAPK - mitogen-activated protein kinase MHPG - 3-methoxy-4-hydroxyphenethylene glycol NE - norepinephrine NMDA - N-methyl-D-aspartate NTS - nucleus tractus solitarius or nucleus of the solitary tract PFC - prefrontal cortex PKA - protein kinase A PTSD - posttraumatic stress disorder RT-PCR - real-time polymerase chain reaction SNS - sympathetic nervous system TMT - trimethylthiazoline TNF-α - tumor necrosis factor
Recommended publications
  • Chronic Stress Makes People Sick. but How? and How Might We Prevent Those Ill Effects?

    Chronic Stress Makes People Sick. but How? and How Might We Prevent Those Ill Effects?

    Sussing Out TRESS SChronic stress makes people sick. But how? And how might we prevent those ill effects? By Hermann Englert oad rage, heart attacks, migraine headaches, stom- ach ulcers, irritable bowel syndrome, hair loss among women—stress is blamed for all those and many other ills. Nature provided our prehistoric ancestors with a tool to help them meet threats: a Rquick activation system that focused attention, quickened the heartbeat, dilated blood vessels and prepared muscles to fight or flee the bear stalking into their cave. But we, as modern people, are sub- jected to stress constantly from commuter traffic, deadlines, bills, angry bosses, irritable spouses, noise, as well as social pressure, physical sickness and mental challenges. Many organs in our bodies are consequently hit with a relentless barrage of alarm signals that can damage them and ruin our health. 56 SCIENTIFIC AMERICAN MIND COPYRIGHT 2003 SCIENTIFIC AMERICAN, INC. Daily pressures raise our stress level, but our ancient stress reactions—fight or flight—do not help us survive this kind of tension. www.sciam.com 57 COPYRIGHT 2003 SCIENTIFIC AMERICAN, INC. What exactly happens in our brains and bod- mone (CRH), a messenger compound that un- ies when we are under stress? Which organs are leashes the stress reaction. activated? When do the alarms begin to cause crit- CRH was discovered in 1981 by Wylie Vale ical problems? We are only now formulating a co- and his colleagues at the Salk Institute for Biolog- herent model of how ongoing stress hurts us, yet ical Studies in San Diego and since then has been in it we are finding possible clues to counteract- widely investigated.
  • Love, Marriage, and Divorce: Newlyweds' Stress Hormones

    Love, Marriage, and Divorce: Newlyweds' Stress Hormones

    Journal of Consulting and Clinical Psychology Copyright 2003 by the American Psychological Association, Inc. 2003, Vol. 71, No. 1, 176–188 0022-006X/03/$12.00 DOI: 10.1037/0022-006X.71.1.176 Love, Marriage, and Divorce: Newlyweds’ Stress Hormones Foreshadow Relationship Changes Janice K. Kiecolt-Glaser Cynthia Bane Ohio State University College of Medicine and Ohio State Ohio State University Institute for Behavioral Medicine Research Ronald Glaser and William B. Malarkey Ohio State University College of Medicine and Ohio State Institute for Behavioral Medicine Research Neuroendocrine function, assessed in 90 couples during their first year of marriage (Time 1), was related to marital dissolution and satisfaction 10 years later. Compared to those who remained married, epinephrine levels of divorced couples were 34% higher during a Time 1 conflict discussion, 22% higher throughout the day, and both epinephrine and norepinephrine were 16% higher at night. Among couples who were still married, Time 1 conflict ACTH levels were twice as high among women whose marriages were troubled 10 years later than among women whose marriages were untroubled. Couples whose marriages were troubled at follow-up produced 34% more norepinephrine during conflict, 24% more norepinephrine during the daytime, and 17% more during nighttime hours at Time 1 than the untroubled. Broadly stated, social learning models suggest that disordered Bradbury’s (1999b) “two factor” hypothesis suggests that aggres- communication promotes poor marital outcomes (Bradbury & sion and aggressive tendencies appear to be a key risk factor for Carney, 1993). Although communication measures have been early divorces, whereas marital communication contributes to the linked to marital discord and divorce across a number of studies, variability in satisfaction in intact marriages.
  • Cortisol-Related Signatures of Stress in the Fish Microbiome

    Cortisol-Related Signatures of Stress in the Fish Microbiome

    fmicb-11-01621 July 11, 2020 Time: 15:28 # 1 ORIGINAL RESEARCH published: 14 July 2020 doi: 10.3389/fmicb.2020.01621 Cortisol-Related Signatures of Stress in the Fish Microbiome Tamsyn M. Uren Webster*, Deiene Rodriguez-Barreto, Sofia Consuegra and Carlos Garcia de Leaniz Centre for Sustainable Aquatic Research, College of Science, Swansea University, Swansea, United Kingdom Exposure to environmental stressors can compromise fish health and fitness. Little is known about how stress-induced microbiome disruption may contribute to these adverse health effects, including how cortisol influences fish microbial communities. We exposed juvenile Atlantic salmon to a mild confinement stressor for two weeks. We then measured cortisol in the plasma, skin-mucus, and feces, and characterized the skin and fecal microbiome. Fecal and skin cortisol concentrations increased in fish exposed to confinement stress, and were positively correlated with plasma cortisol. Elevated fecal cortisol was associated with pronounced changes in the diversity and Edited by: Malka Halpern, structure of the fecal microbiome. In particular, we identified a marked decline in the University of Haifa, Israel lactic acid bacteria Carnobacterium sp. and an increase in the abundance of operational Reviewed by: taxonomic units within the classes Clostridia and Gammaproteobacteria. In contrast, Heather Rose Jordan, cortisol concentrations in skin-mucus were lower than in the feces, and were not Mississippi State University, United States related to any detectable changes in the skin microbiome. Our results demonstrate that Timothy John Snelling, stressor-induced cortisol production is associated with disruption of the gut microbiome, Harper Adams University, United Kingdom which may, in turn, contribute to the adverse effects of stress on fish health.
  • Posttraumatic Stress Disorder

    Posttraumatic Stress Disorder

    TRAUMA AND STRESSOR RELATED DISORDERS POSTTRAUMATIC STRESS DISORDER What it is: In posttraumatic stress disorder, or PTSD, specific mental and emotional symptoms develop after an individual has been exposed to one or more traumatic events. The traumatic event experienced can range from war, as a combatant or a civilian, physical attack or assault, sexual violence, childhood physical or sexual abuse, natural disasters or a severe car accident. The traumatic events do not have to be experienced first-hand for the individual to develop PTSD, it can also develop as a result of witnessing a traumatic event, or through indirect exposure – when a traumatic event happens to a close friend or relative. Symptoms of PTSD can include distressing memories or dreams of the traumatic event, an avoidance of anything that is a reminder of the event, flashbacks of the event, as well as mood changes such as becoming more irritable, aggressive or hyper vigilant. In young children, developmental regression such as loss of language may occur. These symptoms can cause major disruptions and impairment to the individual’s ability to function at home, school and work. Individuals with PTSD are also 80% more likely to have symptoms of at least one other mental disorder, such as depressive, bipolar or substance use disorders. Common Symptoms: The following symptoms must be associated with one or more traumatic events the individual has experienced, witnessed or been indirectly exposed to. 1. Recurring and distressing memories of the event 2. Recurring and distressing dreams relating to the event 3. Dissociative reactions, such as flashbacks, in which the individual may feel or act as if the traumatic event were taking place again 4.
  • Stress and Psychoneuroimmunology

    Stress and Psychoneuroimmunology

    Alternative Journal of Nursing July 2006, Issue 11 Stress and Psychoneuroimmunology Revisited: Using mind-body interventions to reduce stress Madeline M. Lorentz, RN, MSN Stress is a fundamental component of life. It is an unconscious response to a demand and when the demand is perceived as excessive, stress results along with diseases and conditions. Psychoneuroimmunology (PNI) has given importance to the relationship between stress and its physiological effects on the body. Scientists in this growing field have discovered that stress modulates the activities of the nervous, endocrine, and immune systems. Mind-body medicine is developing unconventional methods for coping with stress-related disorders. Nurses are empowered to implement mind-body interventions, such as meditation, imagery, therapeutic touch, and humor, to reduce stress and promote self-control and positive well-being for their patients. To ensure meeting the needs of the entire individual, mind, body and spirit, holistic nurses promote the concept of the mind-body connection. Their practice is based on a holistic view of the patient as they help patients manage their illness; how to think about it, cope with it and respond to it. Holistic approaches in health care hold promise for positive outcomes when the mind-body model is embraced. The concept of mind- body connection may be first attributed to Florence Nightingale who wrote in her Notes on Nursing in 1862 about the healing power of sensory stimulation and personal connection. A new discipline evolved from this type of thinking and is referred to as psychoneuroimmunology (PNI). The growing field of psychoneuroimmunology was established by scientists who were interested in gaining a better understanding of the interrelationship between the mind and body.
  • Anger and Stress Management

    Anger and Stress Management

    Anger and Stress Management CREATED BY UNCHAINED BRAIN, A LOCAL MENTAL HEALTH INITIATIVE FOCUSED ON BRINGING EDUCATION AND SUPPORT TO THE FISHERS COMMUNITY. TO LEARN MORE VISIT UNCHAINEDBRAIN.ORG AND SEE PAGE 3! Anger is an emotion that Stress is a feeling of is antagonism towards emotional or physical someone or something tension. Stress is your that you feel has done body's reaction to a something wrong to you. challenge or demand. Anger can be healthy as Stress can be positive as it is a way to express it helps you avoid negative emotions. danger. 1. Identify triggers a. Structuring your day differently, practicing management techniques 2. Evaluate a. Anger can be sometimes be good and give you the courage to stand up to injustices you see b. Figure out whether your anger is helping or harming others 3. Recognize your physical symptoms a. Racing heartbeat Anger b. Clenching fists c. Face feeling hot/turning red Management 4. Step away a. Remove yourself from a stressful situation b. Don't dodge, just manage 5. Talk to a friend a. Work on developing an answer to a problem versus just venting 6. Changing the "channel" a. Focus on something other than what makes you angry b. Find something that makes it difficult for the angry thoughts to leak in Acute: short term stress that goes away quickly. Everyone experiences acute levels of stress Types of Chronic: Stress lasting for a long period of time. Stress Can go on for weeks or months at a time without realizing you're stressed.
  • Hypothalamic–Pituitary–Adrenal Axis Dysregulation and Behavioral Analysis of Mouse Mutants with Altered Glucocorticoid Or Mineralocorticoid Receptor Function

    Hypothalamic–Pituitary–Adrenal Axis Dysregulation and Behavioral Analysis of Mouse Mutants with Altered Glucocorticoid Or Mineralocorticoid Receptor Function

    Stress, September 2008; 11(5): 321–338 REVIEW Hypothalamic–pituitary–adrenal axis dysregulation and behavioral analysis of mouse mutants with altered glucocorticoid or mineralocorticoid receptor function BENEDICT J. KOLBER, LINDSAY WIECZOREK, & LOUIS J. MUGLIA Departments of Pediatrics and Molecular Biology and Pharmacology and Program in Neuroscience, Washington University in St Louis, St Louis, MO 63110, USA (Received 12 July 2007; revised 29 October 2007; accepted 19 November 2007) Abstract Corticosteroid receptors are critical for the maintenance of homeostasis after both psychological and physiological stress. To understand the different roles and interactions of the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) during stress, it is necessary to dissect the role of corticosteroid signaling at both the system and sub-system level. A variety of GR transgenic mouse lines have recently been used to characterize the role of GR in the CNS as a whole and particularly in the forebrain. We will describe both the behavioral and cellular/molecular implications of disrupting GR function in these animal models and describe the implications of this data for our understanding of normal endocrine function and stress adaptation. MRs in tight epithelia have a long established role in sodium homeostasis. Recently however, evidence has suggested that MRs in the limbic brain also play an important role in psychological stress. Just as with GR, targeted mutations in MR induce a variety of behavioral changes associated with stress adaptation. In this review, we will discuss the implications of this work on MR. Finally, we will discuss the possible interaction between MR and GR and how future work using double mutants (through For personal use only.
  • Are All Chronic Social Stressors the Same? Behavioral, Physiological

    Are All Chronic Social Stressors the Same? Behavioral, Physiological

    https://doi.org/10.24839/2325-7342.JN23.5.376 Are All Chronic Social Stressors the Same? Behavioral, Physiological, and Neural Responses to Two Social Stressors in a Female Mouse Model of Anxiety and Depression Michael R. Jarcho*, Siena College and Loras College; Madeline R. Avery, Loras College; Kelsey B. Kornacker , Danielle Hollingshead, and David Y. Lo*, Coe College ABSTRACT. Chronic stress has been associated with several negative health outcomes and psychopathological conditions, and social stressors (e.g., exclusion from a group, loss of a loved one) can be particularly problematic with regard to psychopathological conditions. Social isolation or instability can result in both behavioral and physiological stress responses. The present study attempted to assess whether the behavioral and physiological markers of stress would follow similar patterns in response to both social isolation and instability. By employing both of these models of social stress in female mice, we hoped to determine which might serve as a more appropriate model of stress-induced anxiety or depression in women. One behavioral index of anxiety, rearing behavior, was elevated only in animals experiencing social instability, F(2, 351) = 6.91, p = .001, η2 = .04, (1-b) = 0.94. Despite small sample sizes, gene expression of proinflammatory markers interleukin one beta receptor and tumor necrosis factor alpha were significantly elevated in hippocampal samples from mice that experienced either social stressor compared to controls, IL1-beta receptor, F(2, 6) = 5.65, p = .045, η2 = .85, (1-b) = 0.99, TNF alpha, F(2, 6) = 8.89, p = .042, η2 = .86, (1-b) = 0.99, with the highest levels in mice that experienced social instability.
  • Depression, Suicide, Inflammation, and Physical Illness

    Depression, Suicide, Inflammation, and Physical Illness

    C HA P TER 1 6 STRESS AND ITS SEQUELAE: DEPRESSION, SUICIDE, INFLAMMATION, AND PHYSICAL ILLNESS George M. Slavich and Randy P. Auerbach Life stress is a central construct in many contem- METHODOLOGICAL ISSUES IN THE porary models of mental and physical health. Con- ASSESSMENT OF STRESS sistent with these formulations, a large corpus of Although there is little debate about whether stress research has demonstrated that stress plays an influ- should be accorded a central role in etiological ential role in the onset, maintenance, and recurrence models of disease, many questions remain regard- of psychiatric illness, as well as in several major ing how to best operationalize and assess life stress. physical health problems that cause substantial Over the past century, researchers have relied most morbidity and mortality (Cohen, Janicki-Deverts, & heavily on self-report checklist measures of stress Miller, 2007; Harkness & Monroe, 2016; Kendler, that have advantages but also several limitations. Karkowski, & Prescott, 1999; Slavich, 2016b). In As a result of these limitations, investigators began this chapter, we summarize key studies on these using interview-based systems to assess life stress important topics with a focus on well-documented that yield extensive information about the differ- effects and lingering conceptual and methodological ent contextual features of reported stressors. These issues. stress assessment methods have been reviewed in To accomplish these goals, we first summarize detail elsewhere (e.g., Cohen, Kessler, & Gordon, how stress has been conceptualized and assessed 1997; Dohrenwend, 2006; Hammen, 2016; over the years. Second, we review links between Harkness & Monroe, 2016; Monroe, 2008; different types of stress exposure and depression, Monroe & Slavich, 2016; Slavich, 2016a).
  • Poverty Raises Levels of the Stress Hormone Cortisol: Evidence from Weather Shocks in Kenya*

    Poverty Raises Levels of the Stress Hormone Cortisol: Evidence from Weather Shocks in Kenya*

    Poverty Raises Levels of the Stress Hormone Cortisol: Evidence from Weather Shocks in Kenya* Johannes Haushofer, Joost de Laat, Matthieu Chemin October 21, 2012 Abstract Does poverty lead to stress? Despite numerous studies showing correlations between socioeconomic status and levels of the stress hormone cortisol, it remains unknown whether this relationship is causal. We used random weather shocks in Kenya to address this question. Our identication strategy exploits the fact that rainfall is an important input for farmers, but not for non-farmers such as urban artisans. We obtained salivary cortisol samples from poor rural farmers in Kianyaga district, Kenya, and informal metal workers in Nairobi, Kenya, together with GPS coordinates for household location and high-resolution infrared satellite imagery meausring rainfall. Since rainfall is a main input into agricultural production in the region, the absence of rain constitutes a random negative income shock for farmers, but not for non-farmers. We nd that low levels of rain increase cortisol levels with a temporal lag of 10-20 days; crucially, this eect is larger in farmers than in non-farmers. Both rain and cortisol levels are correlated with self-reported worries about life. Together, these ndings suggest that negative events lead to increases in worries and the stress hormone cortisol in poor people. JEL Codes: C93, D03, D87, O12 Keywords: weather shocks, rainfall, cortisol, stress, worries *We thank Ernst Fehr, David Laibson, Esther Duo, Abhijit Banerjee, and the members of the Harvard Program in History, Politics, and Economics for valuable feedback; Ellen Moscoe, Averie Baird, and Robin Audy for excellent research assistance; and Tavneet Suri for providing the rainfall data.
  • Oxytocin Mitigates the Negative Consequences of Chronic Social

    Oxytocin Mitigates the Negative Consequences of Chronic Social

    Bucknell University Bucknell Digital Commons Master’s Theses Student Theses 2017 Oxytocin Mitigates the Negative Consequences of Chronic Social Isolation in Prairie Voles (Microtus ochrogaster) Elyse Kathleen McMahon Bucknell University, [email protected] Follow this and additional works at: https://digitalcommons.bucknell.edu/masters_theses Recommended Citation McMahon, Elyse Kathleen, "Oxytocin Mitigates the Negative Consequences of Chronic Social Isolation in Prairie Voles (Microtus ochrogaster)" (2017). Master’s Theses. 187. https://digitalcommons.bucknell.edu/masters_theses/187 This Masters Thesis is brought to you for free and open access by the Student Theses at Bucknell Digital Commons. It has been accepted for inclusion in Master’s Theses by an authorized administrator of Bucknell Digital Commons. For more information, please contact [email protected]. I, Elyse K. McMahon, do grant permission for my thesis to be copied. ii Acknowledgments I would first like to thank my thesis advisor Dr. Mark Haussmann of the Biology Department at Bucknell University. Dr. Haussmann was always available whenever I ran into problems with my research or writing. I would also like to thank my second thesis advisor, Dr. Jennie Stevenson of the Psychology Department at Bucknell University. She was always available for assisting in my animal work and guiding me through writing. Both consistently allowed this paper to be my own work, but steered me in the right the direction whenever they thought I needed it. Their expertises in the fields of Physiology and Neuroscience have kept me motivated to learn more about these areas and better my thesis. With the help and guidance of these two individuals, I will be completing my Master’s thesis with enhanced knowledge not only on stress physiology and aging, but also on the psychological aspects of social isolation.
  • Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone

    Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone

    International Journal of Molecular Sciences Review Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone Tiago Chaves 1,2, Csilla Lea Fazekas 1,2, Krisztina Horváth 1,2, Pedro Correia 1,2, Adrienn Szabó 1,2, Bibiána Török 1,2, Krisztina Bánrévi 1 and Dóra Zelena 1,3,* 1 Laboratory of Behavioural and Stress Studies, Institute of Experimental Medicine, 1083 Budapest, Hungary; [email protected] (T.C.); [email protected] (C.L.F.); [email protected] (K.H.); [email protected] (P.C.); [email protected] (A.S.); [email protected] (B.T.); [email protected] (K.B.) 2 Janos Szentagothai School of Neurosciences, Semmelweis University, 1083 Budapest, Hungary 3 Centre for Neuroscience, Szentágothai Research Centre, Institute of Physiology, Medical School, University of Pécs, 7624 Pécs, Hungary * Correspondence: [email protected] Abstract: Stress adaptation is of utmost importance for the maintenance of homeostasis and, therefore, of life itself. The prevalence of stress-related disorders is increasing, emphasizing the importance of exploratory research on stress adaptation. Two major regulatory pathways exist: the hypothalamic– pituitary–adrenocortical axis and the sympathetic adrenomedullary axis. They act in unison, ensured by the enormous bidirectional connection between their centers, the paraventricular nucleus of the hypothalamus (PVN), and the brainstem monoaminergic cell groups, respectively. PVN and especially their corticotropin-releasing hormone (CRH) producing neurons are considered to be the centrum of stress regulation. However, the brainstem seems to be equally important. Therefore, Citation: Chaves, T.; Fazekas, C.L.; we aimed to summarize the present knowledge on the role of classical neurotransmitters of the Horváth, K.; Correia, P.; Szabó, A.; brainstem (GABA, glutamate as well as serotonin, noradrenaline, adrenaline, and dopamine) in stress Török, B.; Bánrévi, K.; Zelena, D.