The ResearchData@TAMU Digital Catalog

ResearchData@TAMU collects and indexes research data produced by TAMU researchers and stored in data repositories around the world. The catalog increases discoverability of research data in support of re-use, experimental reproducibility, and social impact.

“Open access to research data is critical for advancing science, scholarship, and society. Research data, when repurposed, has an accretive value. Publicly funded research should be publicly available for public good.” - from preamble to the Denton Declaration: An Open Data Manifesto

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Code for "Influence of convection on stratospheric water vapor in the North American Monsoon region"
Diverse Predoctoral Training in Genetics
Cell Biology And Genetics; https://hdl.handle.net/20.500.14641/1258; DHHS-NIH-National Institute of General Medical Science
Texas A&M University has a long history of training in the genetic sciences, with the first graduate degree having been awarded in 1919. The first Interdisciplinary Program (IDP) in Genetics was the first IDP established at Texas A&M in 1983, and has been at the forefront of diversifying not only the trainee pool that will contribute to a diversified workforce, but is also leading in the preparedness of students for diverse career paths. The Genetics IDP preceptors have world-renowned research programs providing unique opportunities for trainees to perform dissertation research in laboratories using cutting-edge technologies that are addressing important and impactful questions in modern genetics that impact human health and well-being, while also having extensive mentoring and career development opportunities. This innovative training program aims to be a model for "preparing diverse scientists for a diverse workforce". The Genetics IDP has developed several initiatives and partnerships that have resulted in a dramatic increase in diversity of applicants and matriculates to the program. Similar to the need for a diverse genetics workforce, efforts are needed to diversify preparedness for future workforce needs and career opportunities. Modern training in genetics and the sub-discipline of genomics not only requires mastering classical Mendelian and quantitative genetics, but expertise in big data, interpersonal interactions that is essential for convergence research, and project management that can be applied to diverse career opportunities. The training program, which will support 4 new trainees each year for 2-year appointments (8 concurrent trainees), is designed to train the next generation of scholar in modern genetics by providing contemporary skills and exposure to the increasingly broad range of career opportunities that these scholars will pursue in order to have a profound impact on the future of genetic sciences. The goals of the training program are to: 1) Provide doctoral students with balanced research and training opportunities that span the continuum from basic science to applied applications and the scientific knowledge needed to excel in modern genetic sciences irrespective of career path; 2) Offer a rigorous didactic training that provides the fundamentals in Mendelian and quantitative genetics, statistics and experimental design, rigor and reproducibility, biostatistics, big data computation skills, and a core set of competencies in communication, interpersonal interactions, and leadership and team science that will be required for successful careers in academia, industry and government; and 3) Ensure that trainees develop appreciation for, familiarity with, and exposure to various career opportunities for well-trained geneticists through mentorship and introduction to experts in various fields.
Dissecting the role of the bed nucleus of the stria terminalis in avoidant behavior.
Psychology; https://hdl.handle.net/20.500.14641/1259; DHHS-NIH-National Institute of Mental Health
Avoidance is a hallmark symptom contributing to the deleterious impact of many anxiety disorders. Despite this, there are major gaps in our understanding of the neural circuits underlying avoidant behavior. A mechanistic account of this key symptom would advance progress toward brain-based innovations for the treatment of pathological anxiety. Signaled active avoidance (SAA) is a behavioral procedure for rats in which a highly persistent avoidance response is triggered by a conditioned stimulus (CS) associated with an aversive unconditioned stimulus (US). Because the avoidance response prevents US delivery, acquisition of SAA causes the US to transition from an imminent threat early in training to a remote threat later in training, once the response has become more frequent. Ethologically inspired models for aversive emotion suggest that this change in threat imminence is consistent with a shift from fear to anxiety, indicating that SAA expression is mediated by an anxiety-like state. The overarching hypothesis of this proposal is that neural circuits of anxiety-like behavior play a central role in SAA. Previous work implicates the bed nucleus of the stria terminalis (BNST) in anxiety. To generate preliminary data for the overarching hypothesis of this proposal, an initial experiment was conducted using an inhibitory DREADD (designer receptor exclusively activated by designer drugs) to inactivate BNST neurons in rats performing SAA. This manipulation demonstrated that BNST is necessary for the maintenance of the avoidance response. The proposed studies will build on this result by dissecting the function of a circuit mechanism for active avoidance, comprised of BNST and key regions that provide it with synaptic input (prefrontal cortex, basal amygdala). Given that avoidant coping is a behavioral disturbance common to many anxiety disorders, this work has clear relevance to public health. Discovery of an avoidance circuitry could provide a novel target for innovative therapeutic interventions for pathological anxiety. The goal of this work is to generate rigorous preclinical data that accelerates clinical advancement.
Function of glutamate delta-1 receptor
Psychiatry Bryan College Station Campus; https://hdl.handle.net/20.500.14641/1260; DHHS-NIH-National Institute of Mental Health
The delta family of ionotropic glutamate receptors consisting of glutamate delta 1 (GluD1) and glutamate delta 2 (GluD2) are unusual since they do not exhibit typical ligand-gated ionic currents. Instead, they are endowed with synaptogenic property by forming a trans-synaptic GluD-Cerebellin1 (Cbln1)-Neurexin complex and inducing synapse formation. In addition, the GluD receptors have C-terminal interactions which may stabilize postsynaptic density machinery and contribute to synaptic plasticity. Although the function of GluD2 subunit in the formation and plasticity of parallel fiber-Purkinje cell synapse in the cerebellum is well established the role of GluD1 enriched in the forebrain remains largely unknown. This has important implications for our understanding of neurodevelopmental and schizoaffective disorders since GRID1 gene that codes for GluD1 is strongly associated with autism, schizophrenia, bipolar disorder and major depression. In addition, Neurexin1 is also highly associated with mental disorders and both Cbln1 and Neurexin1 splice variant levels change in an activity-dependent manner and are therefore susceptible to pathological insult. Thus, the GluD1-Cbln1-Neurexin complex is a highly vulnerable node for emergence of neurocognitive disorders. GluD1 is enriched in the striatum which receives strong excitatory inputs from the cortex and thalamus. Our preliminary results demonstrate a critical role of GluD1 in excitatory neurotransmission in medium spiny neurons in the striatum. Our goal is to address potential cell-type and synapse-selectivity in this effect upon loss of GluD1 which will support its role as a synaptic organizer. We will pursue the following specific aims; (i) Determine the ultrastructural localization of GluD1 in the striatum and the effect of GluD1 loss on synaptic structure. We will use a range of complementary electron microscopy, immunohistochemistry and biochemistry methods to analyze distribution of GluD1 in the striatum and impact of GluD1 loss on striatal synapses and potential reorganization of synaptic components. (ii) Determine the role of GluD1 in synaptic neurotransmission and plasticity. We will use conventional electrophysiology together with ex vivo optogenetics to stimulate specific synapses to address potential synapse-specific roles of GluD1. (iii) Determine the role of striatal GluD1 in cognitive and behavioral control. We will address the impact of changes in synaptic function upon loss of striatal GluD1 on emotional, cognitive and motor behaviors that are regulated by striatal circuits. These studies will be complemented with DREADD technique to manipulate specific striatal pathways. Together, the proposed studies will systematically address the synaptic organizational principle of GluD1 in the striatum and address its role in synaptic and behavioral phenotypes relevant to neuropsychiatric and neurological disorders.
Glucocorticoid modulation of contextual processing and its neurocircuitry: Testing a new model of PTSD pathophysiology
Psychiatry Bryan College Station Campus; https://hdl.handle.net/20.500.14641/413; DHHS-NIH-National Institute of Mental Health
Fifty to 90% of Americans are exposed to trauma that can lead to Post-traumatic Stress Disorder (PTSD). Only a few develop PTSD. Identifying the vulnerable and modifying the processes that translate risk into illness could reduce the public health burden of this serious disease. Risk factors and neurobiological mechanism are being identified, but much remains unknown. Emerging models identify relevant genes, environments, brain circuits and behavior, expanding our focus beyond simple fear learning to incorporate more complex neural circuits that modulate responses to threat. Studying these circuits and their functions has generated a novel model of PTSD pathophysiology that focuses on deficits in context processing (CP) and on the hippocampal- prefrontal circuitry that subserves CP functions. This model is supported by growing evidence, explains much of PTSD's phenomenology, and integrates much of its neurobiology. The aim of this project is to further develop and test this model, and explore implications for treatment and, potentially, for prevention. PTSD patients respond fearfully to ambiguous cues (e.g., loud noise) even when in safe contexts (e.g., home backyard). Difficulty linking cues to contexts may be a core problem for them, undermining access to contextual information that should modulate adaptive responses. The hippocampus (Hpc) plays a key role in this process, mediating core CP functions like pattern separation (PS) and pattern completion (PC). PS/PC deficits may underlie CP difficulties in PTSD, contributing to an inability to remember that something once threatening is now safe (extinction recall) or to recognize potential danger when danger signals are contextual (fear renewal). Glucocorticoid (GC) signaling in Hpc can impair CP functions, so evidence of increased GC receptor sensitivity in PTSD is consistent with the CP model. Genetic and developmental factors known to shape GC sensitivity may contribute to PTSD risk through impact on CP functions like PS/PC, perhaps mediated by activity/connectivity within Hpc-prefrontal (PFC) circuits. This project will test the CP model, examining links between CP functions like PS/PC and the Hpc-PFC neural pathways subserving these functions, the role of glucocorticoid signaling in moderating these pathways and functions, and the ability of GCs to improve or undermine CP functions. It will do so by studying 120 healthy subjects performing PS/PC and fear learning tasks in fMRI, under low cortisol, physiological cortisol, and elevated (moderate and high) cortisol levels. “Baseline” levels of GC signaling will be assessed via integrated cortisol secretion (hair cortisol) and GC receptor sensitivity (in vitro lysozyme inhibition). The project will also study 150 PTSD patients in the same paradigm, to determine whether PS/PC processes are core deficits in PTSD, linked to symptom severity and extinction recall/fear renewal deficits via Hpc-PFC dysfunction, and to test the ability of GCs to “rescue” CP deficits in PTSD, via impact on Hpc-PFC pathways.