Browsing by Department "Psychology"

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Components of Selection History and the Control of Attention
Psychology; https://hdl.handle.net/20.500.14641/1074; DHHS-NIH-National Institute On Drug Abuse
PROJECT SUMMARY/ABSTRACT Attention selects which aspects of sensory input receive cognitive processing and thereby influence behavior. Drug addiction alters the attentional system, resulting in prominent attentional biases towards drug cues. Such drug-related attentional biases are related to the broader phenomenology of addiction, including craving and relapse. There has been long-standing interest in implementing attentional bias measures in clinical settings, either as a predictive measure to inform treatment decisions or as a target of treatment. However, a major barrier to the realization of this goal is that current means of assessing these biases are not sufficiently precise to support clinical utility, which has stifled progress in this area. Mirroring this complexity, and underscoring the need for clarity, debate has arisen concerning the role of learning history in the guidance of attention more broadly. Persistent attentional biases have been linked to reward history, learning from aversive outcomes, and outcome-independent selection history (e.g., familiarity). Emerging accounts of such experience-dependent attentional biases disagree about the nature of the underlying mechanism(s) involved. If we do not understand the variety of influences of learning history on attention at a fundamental level, how can we understand how these influences contribute to addiction-related attentional biases? The proposed research directly addresses this need by identifying, isolating, and measuring multiple hypothesized components of the attentional biases that characterize addiction, providing the precision necessary for more accurate predictions of patient outcomes and more targeted efforts to improve these outcomes through attentional bias modification. Specific Aim 1 will distinguish between common and distinct attentional priority signals arising from reward learning and reward-independent selection history, probing both the cognitive and neural mechanisms underlying each of these sources of priority. Specific Aim 2 will identify the cognitive profile and neural mechanisms underlying attentional biases attributable to aversive conditioning, which together with Specific Aim 1 will provide a comprehensive picture of the multifaceted nature of experience-dependent attention. The overarching goal of the proposed research is to characterize multiple distinct components of experience-dependent attentional bias that contribute to attentional biases evident in drug-dependent individuals. These fundamental components of attentional bias will provide a much more precise window into the attentional processes that are relevant to our understanding of addiction than existing measures can offer. It is anticipated that the knowledge gained from the proposed research with provide a foundation for overcoming fundamental limitations in the clinical utility of attentional bias measures, allowing for fruitful exploration of this aspect of addiction in the context of improving assessment and treatment.
Exploring Striatal Circuits Underlying Behavioral Flexibility During Punishment of Cocaine Seeking
Psychology; https://hdl.handle.net/20.500.14641/1103; DHHS-NIH-National Institute of Neurological Disorders and Stroke
Abstract A hallmark of drug addiction is the uncontrollable urge to seek drug despite negative consequences— drug seeking individuals become resistant to punishment. Punishment resistance has also been observed in an animal model of addiction. In this model, some rats continue to seek cocaine despite a footshock outcome (i.e., punishment), whereas other rats instead reduce their cocaine seeking to avoid footshock. The propensity to reduce cocaine seeking to avoid a negative consequence may require behavioral flexibility, an adaptive form of learning that allows changes in behavior in response to new features in the environment. Previous work using measures of behavioral flexibility, such as reversal learning and strategy shifting, have shown that striatal circuits are essential for expressing behavioral flexibility. Specifically, frontal cortex areas such as the orbitofrontal cortex (OFC) and thalamic areas such as the parafascicular thalamus (PF) target the dorsal striatum (DS) and help track events in the environment that are important for updating behavior. One striatal cell type that is important for the role of PF and OFC in behavioral flexibility are cholinergic interneurons (CIN). However, the role of be- havioral flexibility and its neural substrates in punishment resistance is poorly understood. The proposed work will test the hypothesis that punishment-resistant cocaine seeking results from reduced behavioral flexibility when faced with negative consequences. Specific Aim 1 (F99, dissertation phase) will identify a DS CIN mechanism that supports behavioral flexibility during punishment of cocaine seeking in rats, using immunohistochemistry, behavioral pharmacological, and optogenetics. Specific Aim 2 (K00, postdoctoral phase) proposes a research direction that will focus on the role of OFC in driving vs suppressing punishment-resistant cocaine seeking, which serves as an extension of the dissertation work that will be completed in Aim 1. I will acquire technical skills related to a measure of neurotransmission, such as in vivo calcium imaging, to fully investigate OFC activity patterns related to cocaine seeking in the face of negative outcomes. In addition, Aim 2 describes the qualities I will seek in a postdoctoral mentor and research environment that can support my research interests, technical training goals, and growth as an independent neuroscientist. Overall, the proposed research in this training fel- lowship aims to define the neural mechanisms underlying reduced behavioral flexibility, which will contribute to identifying targeted treatment strategies for drug addiction.
Neural Circuits for Stress-Impaired Extinction Learning
Psychology; https://hdl.handle.net/20.500.14641/1089; DHHS-NIH-National Institute of Mental Health
Project Summary Clinical disorders of fear and anxiety, including trauma- and stressor-related disorders, represent an enormous public health burden. Cognitive-behavioral therapies, such as prolonged exposure therapy, have proven to be remarkably effective in reducing pathological fear in patients with these disorders. Nonetheless, there are a number of factors that limit the efficacy of exposure therapy. In particular, stress undermines exposure-based therapies by impairing extinction learning and promoting fear relapse. Despite years of work elucidating the neural circuitry for extinction, the neural mechanisms responsible for stress-induced extinction impairments remain poorly understood. One possibility is that stress dysregulates neuronal activity in the medial prefrontal cortex (mPFC), a brain area that is critical for extinction learning. In support of this possibility, we have recently shown that footshock stress causes lasting decreases in the spontaneous firing of neurons in the infralimbic (IL) division of the mPFC in rats. Decreases in IL firing were associated with an “immediate extinction deficit” (IED), an extinction impairment that occurs when extinction is performed soon after fear conditioning (a stressor). Importantly, systemic administration of propranolol, a ß-noradrenergic receptor antagonist, prevented both the stress-induced depression of IL firing and the IED, suggesting a role for locus coeruleus norepinephrine (LC-NE) in this phenomenon. Although these data reveal that noradrenergic transmission is involved in the stress-induced depression of mPFC firing, the neural circuit by which stress perturbs mPFC firing is unknown. Interestingly, we have found that propranolol rescues the IED when delivered to the basolateral amygdala (BLA), but not the IL. Based on this work, we propose a novel hypothesis that stress-induced NE release from the LC recruits an inhibitory BLA->IL circuit that dampens activity in IL principal neurons to impair the acquisition and retention of long-term extinction memories. We propose three specific aims to test this hypothesis using a combination of in vivo electrophysiology, functional circuit tracing, and pharmacogenetic manipulations (e.g., `designer receptors exclusively activated by designer drugs' or DREADDs). The first specific aim of the project examines whether LC-NE projections to the IL or BLA are necessary and sufficient for stress-induced changes in mPFC firing and extinction learning deficits. The second specific aim examines explores whether BLA neurons projecting to the IL or PL mediate these effects. The third specific aim determines whether parvalbumin interneurons (PV-INs) in the mPFC are recruited by LC- NE activation and mediate the immediate extinction deficit through feed forward inhibition by BLA afferents. The outcomes of these aims will advance a novel circuit mechanism for stress-induced extinction impairments. Understanding this mechanism will facilitate the development of novel pharmacotherapeutic approaches that optimally engage mPFC circuits to facilitate extinction learning under stress.
Neural Substrates of Contextual Memory in Fear Extinction
Psychology; https://hdl.handle.net/20.500.14641/1089; DHHS-NIH-National Institute of Mental Health
PROJECT SUMMARY Therapeutic interventions, such as exposure therapy, reduce pathological fear in patients with anxiety disorders. Extinction is a fundamental form of learning that underlies these therapies. A major challenge to extinction-based therapies is that the fear reduction is often transient and bound to the place or context in which therapy occurs. For example, when patients confront phobic objects or reminders of trauma outside of the clinic, their fear often relapses. This reveals that extinction learning does not erase fear memory, but yields a context-dependent “safety” memory that inhibits the expression of fear in the place where it is learned. Accordingly, the long-term goal of this project is to understand the neural substrates of fear extinction and relapse, particularly the specific brain circuits involved in the contextual control of extinction. Work in the current funding period of this project has focused on renewal, a relapse of extinguished fear outside the extinction context. Importantly, it was found that the hippocampus (HPC) mediates renewal by inhibiting retrieval of extinction memories encoded by the infralimbic (IL) cortex. In the extinction context, the suppression of conditioned fear is thought to involve IL inhibition of amygdala neurons encoding fear memory. However, recent data challenge this notion—silencing prefrontal-amygdala projections does not impair extinction retrieval. Hence, the precise mechanism for suppressing fear after extinction is still unknown. Recent work on this project suggests a novel alternative: the mPFC may suppress the reactivation of hippocampus-dependent fear memories to facilitate context-dependent extinction memory retrieval. The mPFC projects to the HPC via the thalamic nucleus reuniens (RE), and RE inactivation or chemogenetic silencing of mPFCgRE projections impairs the expression of extinction. Based on this work, it is hypothesized that the RE mediates mPFC-HPC interactions required for context-dependent retrieval of extinction memories. This hypothesis will be tested in three specific aims. The first aim explores whether the mPFC, particularly IL, suppresses the retrieval of extinguished fear memories via RE projections to the HPC. The second aim examines whether the activity of HPC ensembles representing fear and extinction memories are regulated by the RE. The third aim determines whether the RE coordinates oscillatory synchrony in HPC and mPFC during extinction retrieval. The proposed work will elucidate the specific neural circuits mediating the expression of extinction and has important clinical implications for developing therapeutic interventions that target these neural circuits to promote fear suppression and oppose relapse.
Nociceptive (Pain) Input After Spinal Cord Injury (SCI) Enhances Secondary Injury: Identifying Treatments That Can Be Translated to Clinical Practice
Psychology; TAMU; https://hdl.handle.net/20.500.14641/367; DOD-Army-Medical Research Acquisition Activity
Spinal cord injury (SCI) brings a high cost, both in terms of medical treatment and the individual's long-term wellbeing. The degree of injury depends upon both the initial tissue damage (primary injury) and the subsequent loss of tissue in the surrounding region (secondary injury). It is now recognized that nearly half the cell loss is due to secondary injury. Because the processes that contribute to secondary injury unfold over the course of hours to days, it represents a treatable clinical target. Our work has shown that pain input after injury can expand the area of secondary injury, amplifying tissue loss and undermining long-term recovery. This is an important observation, because many spinal cord injuries, especially in military action, are accompanied by additional tissue damage (polytrauma) that will engage pain fibers. If these wounds are at, or below, the level of the SCI, the sensory signals may generate little ¬"psychology" pain (because neural transmission to the brain is disrupted). The sensory signals can, however, still engage neurobiological processes within the spinal cord that influence tissue loss. Of particular concern, our work has shown that incoming pain signals can drive a state of over-excitation that fuels cell death and leads to a breakdown in the blood-spinal cord barrier (BSCD). This barrier normally keeps red blood and other cells from infiltrating the neural tissue (while allowing essential nutrients to pass). When the barrier is broken, hemoglobin leaks out of the blood vessels into the surrounding tissue, causing an area of hemorrhage that kills neurons and non-neuronal cells (e.g., the oligodendrocytes that ensheathe axons within the white matter). This, in conjunction with an amplified immune response, could feed a rise in pro-inflammatory cytokines that leads to further cell loss. Acting together, the hemorrhage will expand the region of secondary injury and thereby undermine long-term recovery. Pain input after SCI appears to fuel hemorrhage in two ways. One is by engaging a signal pathway that leads to the death of the endothelial cells that form the BSCD. This process is known as progressive hemorrhagic necrosis. It can be identified by the activation of particular proteins (e.g., Sur1-Trpm4) and the fragmentation of capillaries. The second key process involves an increase in blood pressure (hypertension). Interestingly, this cardiac event is not due to a local (spinally-mediated) effect (as occurs, for example, in autonomic dysreflexia). Instead, new research has revealed that pain-induced hypertension and hemorrhage depend upon brain systems. Supporting this, we have shown that cutting the surviving fibers blocks the adverse effect of noxious stimulation. Inhibiting brain function (via a medically induced coma) also has a protective effect. These surprising data suggest that secondary tissue loss after SCI depends, in part, on brain systems. Interestingly, blocking "psychological" pain with an opiate analgesic (morphine) does not counter the adverse effect of stimulation. This suggests that the damage is due to engaging the underlying neural processes, not the resultant experience of pain. New work has shown that this neural activity can be blocked by inhibiting cellular activity within the spinal cord using the local anesthetic lidocaine. A limitation of past studies is that sensory fibers were artificially driven using a brief period (6 minutes) of intermittent electrical stimulation. New data has shown that selectively engaging pain fibers, by applying the irritant capsaicin (the active ingredient of chili peppers), leads to a prolonged period of hemorrhage after SCI and undermines long-term recovery. The present proposal will use this treatment to explore the circumstances under which pain input affects tissue loss and the neurobiological mechanisms that underlie this effect. More importantly, we seek to show how two treatments can be used to reduce the adverse effects of pain input on injury. We propose that inducing a coma-like state with pentobarbital will attenuate hemorrhage after injury. We also propose that blocking neural conduction along spared fibers, by slowing infusing lidocaine into the spinal cord above the injury, will reduce capsaicin-induced hemorrhage. The benefits of these manipulations will be evident from a reduction of hemoglobin infiltration and reduced expression of proteins associated with cell death and inflammation. We focus on the beneficial effects of general anesthesia and spinally applied lidocaine because these treatments can be readily translated to clinical practice. Indeed, our work suggests that epidural lidocaine given soon after injury could provide both relief from pain and halt the pain-induced expansion of secondary injury. Because nearly all military-related SCI involve polytrauma, this treatment could become a standard of care. This treatment is routinely used to attenuate pain during child birth. Risks are minimal. The potential benefits are high. Given additional empirical data, mapping out treatment effectiveness, the procedures we explore could be rapidly transitioned to humans. The heuristic is that, if we can spare just 10% of the ascending/descending fibers, the person will walk out of the hospital. Implementing these procedures could help meet this goal, and thereby dramatically improve long-term quality of life.
SBP: Collaborative Research: Gender Discrimination in Hiring for STEM Graduates
Psychology; TAMU; https://hdl.handle.net/20.500.14641/327; National Science Foundation
This interdisciplinary project will use cutting-edge technology to study the labor market for computer science graduates in Science, Technology, Engineering, and Mathematics (STEM) fields. Although women?s share in STEM employment has been growing in non-computer science occupations, their share in computer science occupations has been declining since the 1990s. Because computer science occupations account for 50% of STEM workers, this decline is slowing the growth of women?s share in STEM fields overall, and suggests significant untapped potential that could improve US productivity and competitiveness. One reason that women may not seek out or remain in computer science fields is that they are treated differently than men during the hiring process. This project uses a laboratory experiment in the field on first-line hiring managers to determine first if there is differential treatment of women in hiring recent computer science graduates. If there is such a difference, it will determine the characteristics of women who are more likely to be treated negatively as well as general characteristics of firms that are more likely to exhibit differential treatment. Resumes will be randomly generated to include different characteristics that, if their inclusion helps women more than men, will indicate potential reasons for this differential treatment. The experiment will also use eye-tracking to determine how recruiters visually process computer science resumes and whether or not there are differences between how they process male vs. female resumes. These combined results will help to differentiate between economic theories of discrimination, and will advance social science by increasing our theoretical understanding of when and how differential treatment occurs. Results from this study can be used to make recommendations to individuals applying for these positions and institutions which advise them, to employers who desire to hire the best candidates, and to policy makers who want to increase meritocratic hiring in STEM. The results will thus lead to a more diverse and competitive workforce, increasing the economic competitiveness of the U.S. This project combines two cutting-edge methodologies, eye-tracking and resume-randomization, to study gender discrimination at the first stage of the STEM hiring process. It will determine if there is differential treatment by gender in how first-line hiring managers treat resumes, whether the treatment is similar or different along the applicant quality distribution, and if there are industry characteristics (ex. firm size, industry code) that would lead to higher or lower levels of differential treatment. Finally, this study will differentiate between different theories of statistical and taste-based discrimination. Technical recruiters in charge of first-line interview decisions will be solicited at university recruitment fairs and industry fairs to view and process hypothetical resumes for Computer Science majors. They will be asked to follow their standard hiring practice and to choose resumes to ?move to the next stage.? The resumes will then be redisplayed and participants will rate each resume and give the expected starting salary and position. While participants are viewing the resumes, their eye-movements will be tracked via an eye-tracking device. Following the resume rating exercise, they will answer a short demographic survey. Resumes with randomized inputs based on actual resumes will be created via a randomization program. Outcomes of interest include information on ratings, moving the resume to the next stage, position placement, salary ranges, time spent on individual resumes, time spent on and number of looks at specific parts of resumes. The coefficients and significance on the coefficient of gender determine whether or not there is differential treatment by gender, and if so, for which women and by what kinds of firms. Time spent on resumes by gender interacted with differential treatment findings provide information on use of heuristics in the decision-making process. Time spent viewing specific parts of the resume (areas of interest or AOI) and tracking the order that recruiters view parts of the resume provide insight into their decision-making processes. Gender interactions with randomized inputs that support or contradict stereotypes will be used to test employee taste-based discrimination and levels-based statistical discrimination. Position placement by gender will test customer taste-based discrimination. Comparing predicted outcomes with actual outcomes by gender of resume be used to test variance-based statistical discrimination. This project directly impacts the full participation of women in STEM and will (1) improve the well-being of individuals in society, (2) develop a diverse and competitive workforce and (3) increase economic competitiveness. Results from this study can be used to make recommendations to individuals applying for these positions and the institutions who advise them, to employers who desire to hire the best candidates, and to policy makers who want more women and minorities in STEM. The methodology will (4) promote future research on other hiring and discrimination questions. In addition, this project will (5) incorporate graduate and undergraduate students, involving them in cutting-edge research and providing them with a platform to undertake their own independent work. Graduate and undergraduate students will receive mentoring and research skills, increasing their attractiveness to employers and advanced degree programs.
Time Lag as a Moderator of Parental Control and SES and Child Anxiety Outcomes
Psychology; TAMU; https://hdl.handle.net/20.500.14641/503; DHHS-NIH-National Institute of Mental Health
Project Summary Roughly one-third (31.8%) of adolescents will be diagnosed with an anxiety disorder 1, with as many as 20% of young children already showing symptoms that will predict problems across their lifetime 2, 3. Substantial time and effort have resulted in a growing literature on the development of anxiety in childhood. Multiple contextual contributors to risk for anxiety problems have been identified, including parental behaviors 15,16, developmental age 17, and socioeconomic status 18. Parenting behaviors 15, 19, 20, parental control in particular15, and socioeconomic disadvantage18, 21, 22, predict increased risk for anxiety problems across development and comprise a substantial portion of the available literature evaluating the influence of context on childhood anxiety. Yet, the search continues for precisely how environment-based risk for anxiety unfolds across childhood, ultimately manifesting in child symptoms 12, 15. Significant effort has been placed on understanding the mechanisms of anxiety risk 23–25 and how to either treat or modify these mechanisms 8, 10. Critically, the timing by which context “gets under the skin” and ultimately results in elevated anxiety in children has been relatively ignored, perhaps as a result of adopting standard time lags in developmental research (6-12 months between assessments) and/or the absence of sophisticated statistical techniques that allow for tests of time lag as a key variable. The absence of such work has likely resulted from limited methods for considering the ways that temporal lag can moderate effects sizes. The work of this fellowship will include testing the role of temporal lag in the link between parental control (study aim #1) and SES (study aim #2) and anxiety symptoms during more and less sensitive periods of development. This work will also provide an important basis for understanding anxiety development across childhood and inform both subsequent empirical designs and the development of targeted programs of prevention in schools, homes, and communities. The current project is designed with an integrated training plan that will prepare the fellowship applicant for a future career as an independent interdisciplinary researcher. The three overarching training goals are: (1) Learn to conduct and disseminate work rooted in lag as a moderator meta-analysis (LAMMA), (2) build a foundational knowledge in adolescent development, and (3) advance Tristin’s professional development to facilitate an interdisciplinary researcher career. These training goals will effectively prepare the applicant for a future research career and lay the foundation for future research using LAMMA and examining anxiety trajectories across childhood as this development is related to contextual factors.