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Craig M. Powell - US grants
Affiliations: | University of Texas Southwestern Medical Center, Dallas, TX, United States |
Area:
Learning and Memory, Mouse Models of AutismWebsite:
http://www8.utsouthwestern.edu/utsw/cda/dept14802/files/242109.htmlWe are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Craig M. Powell is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
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1992 — 1996 | Powell, Craig M | F30Activity Code Description: Individual fellowships for predoctoral training which leads to the combined M.D./Ph.D. degrees. |
Persistent Kinase Activation in Long Term Potentiation @ Baylor College of Medicine |
0.907 |
2003 — 2007 | Powell, Craig M | K08Activity Code Description: To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Bdnf in Depression, Antidepressant Action, and Memory @ University of Texas SW Med Ctr/Dallas [unreadable] DESCRIPTION (provided by applicant): The neurologic basis of depression and response to antidepressant treatment remain uncertain. Recent evidence suggests that the brain derived neurotrophic factor (BDNF) is increased by administration of various classes of antidepressant treatments and BDNF infusion into the brain has antidepressant effects in animal models. Furthermore, BDNF's role in acute regulation of synaptic transmission and synaptic plasticity in the hippocampus and other areas, implicates a role in learning and memory paradigms. The proposed studies will examine the role of BDNF in the adult brain in depression and response to antidepressant treatments. These studies will also screen BDNF deficient mice for deficits in two learning and memory paradigms. We hypothesize that mice lacking BDNF in the brain will exhibit increased susceptibility stress effects in animal models of depression and that these mice will be less susceptible to beneficial effects of anitidepressant therapy. We further hypothesize that mice lacking BDNF in the brain will exhibit deficits in learning and memory paradigms. Finally, we will examine the role of BDNF in support of monoaminergic and serotonergic projections in the adult brain. These studies will enhance our understanding of the pathophysiology of depression and mechanisms of antidepressant action. This knowledge may lead to new therapeutic targets in depression. Experiments examining the role of BDNF in spatial and emotional learning and memory will further our understanding of how neurotrophic factors can influence learning and memory and may lead to new therapeutic considerations in clinical disorders of memory such as Alzheimer's disease. To date, studies examining the role of BDNF in behavioral paradigms have been difficult due to the early postnatal lethality and sensory abnormalities of constitutive BDNF knockout mice. Our approach will be to make use of brain-directed, inducible BNDF knockout mice that have been generated in the Nestler laboratory. This system avoids developmental and peripheral effects of traditional knockout approaches. We also propose to make use of focal injection of Cre-expressing AAV vectors into flox-BDNF mice to assess the specific brain subregions involved with greater temporal specificity. [unreadable] [unreadable] |
0.957 |
2004 — 2006 | Powell, Craig M | K08Activity Code Description: To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Bdnf in Depression, Antidepressant Action, and Memory. @ University of Texas SW Med Ctr/Dallas [unreadable] DESCRIPTION (provided by applicant): The neurologic basis of depression and response to antidepressant treatment remain uncertain. Recent evidence suggests that the brain derived neurotrophic factor (BDNF) is increased by administration of various classes of antidepressant treatments and BDNF infusion into the brain has antidepressant effects in animal models. Furthermore, BDNF's role in acute regulation of synaptic transmission and synaptic plasticity in the hippocampus and other areas, implicates a role in learning and memory paradigms. The proposed studies will examine the role of BDNF in the adult brain in depression and response to antidepressant treatments. These studies will also screen BDNF deficient mice for deficits in two learning and memory paradigms. We hypothesize that mice lacking BDNF in the brain will exhibit increased susceptibility stress effects in animal models of depression and that these mice will be less susceptible to beneficial effects of anitidepressant therapy. We further hypothesize that mice lacking BDNF in the brain will exhibit deficits in learning and memory paradigms. Finally, we will examine the role of BDNF in support of monoaminergic and serotonergic projections in the adult brain. These studies will enhance our understanding of the pathophysiology of depression and mechanisms of antidepressant action. This knowledge may lead to new therapeutic targets in depression. Experiments examining the role of BDNF in spatial and emotional learning and memory will further our understanding of how neurotrophic factors can influence learning and memory and may lead to new therapeutic considerations in clinical disorders of memory such as Alzheimer's disease. To date, studies examining the role of BDNF in behavioral paradigms have been difficult due to the early postnatal lethality and sensory abnormalities of constitutive BDNF knockout mice. Our approach will be to make use of brain-directed, inducible BNDF knockout mice that have been generated in the Nestler laboratory. This system avoids developmental and peripheral effects of traditional knockout approaches. We also propose to make use of focal injection of Cre-expressing AAV vectors into flox-BDNF mice to assess the specific brain subregions involved with greater temporal specificity. [unreadable] [unreadable] |
0.957 |
2009 — 2010 | Powell, Craig M | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Novel Genetic Animal Models of Autism @ Ut Southwestern Medical Center DESCRIPTION (provided by applicant): Autism spectrum disorders (ASDs) are common, debilitating disorders affecting social interaction, communication, and repetitive behaviors. Recent genetic findings have identified mutations in synaptic cell adhesion genes and genes encoding their interacting protein partners at central synapses as genetic causes of autism spectrum disorders. We propose to create novel autism model mouse lines. We will produce both a conditional knockout as well as a global, complete knockout of this synaptic autism gene to mimic complete gene deletion, the most common mutation of this gene linked to autism. Our progress to date is substantial in that we have now demonstrated germline transmission of our conditional knockout construct, thereby establishing founders for both conditional and global knockout lines. We now propose to expand these novel autism model mouse lines and perform initial molecular, biochemical, electrophysiologic and behavioral characterization. In particular, we will measure behaviors corresponding to each of the three core symptom domains in autism spectrum disorder in these mouse lines. The result will be a novel genetic model mouse line of autism, behavioral relevance of the model to autism, and initial studies on brain function using electrophysiology to understand effects on cortical synapses. PUBLIC HEALTH RELEVANCE: Our goal is to better understand a genetic cause of human autism and to use animal models of such causes to identify treatments. This 2-year R21 proposal capitalizes on our significant progress toward creating a novel animal model of autism and will allow us to rapidly advance this project in a brief period. The marriage of our understanding of brain pathology with behavioral abnormalities in these mice will lead to testable hypotheses regarding pharmacologic treatment of autism symptoms in the model and ultimately in autistic patients. |
0.993 |
2009 — 2013 | Powell, Craig M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Neuroligin Function in Vivo: Implications For Autism and Mental Retardation @ Ut Southwestern Medical Center Loss-of-function mutations in members of the neuroligin (NL) family of trans-synaptic cell adhesion molecules have been implicated in human autism and mental retardation. Animal models of autism have been severely limited, but these human genetic findings provide a novel path to develop bona fide mouse models of at least a subtype of human autism or mental retardation. NLs are postsynaptic transmembrane proteins that bind presynaptic beta-neurexins to induce formation of excitatory and inhibitory synapses and to control excitatory/inhibitory (E/I) synapse balance in cultured neurons. Alterations in E/I balance have been proposed as important in pathogenesis of autism and mental retardation. The precise role of NL in vivo and in neurobehavioral abnormalities in autism and mental retardation, however, remains to be determined. We will determine the role of neuroligin in vivo using electrophysiologic and behavioral characterization of NL knockout, human disease mutation knockin, and, in follow-up studies, conditional knockout mice. The driving hypothesis is that mice deficient in NL genes, or carrying known disease-linked mutations in NL, will exhibit behavioral differences consistent with those in human autism or mental retardation, and that these behavioral differences will be associated with specific abnormalities in E/I balance or synaptic function in cortical circuits in vivo. The following specific aims will be addressed: 1. To determine whether NL3 disease-linked mutation or deletion of NL3 result in autism and mental retardation-related behavioral abnormalities. 2. To determine whether deletion of NL3 or NL3 disease-linked mutations result in altered excitatory and inhibitory synaptic connectivity and function. 3. To determine whether deletion of NL3 or NL3 disease-linked mutations alter the threshold for inducing NMDA-receptor-dependent synaptic plasticity in the hippocampus. |
0.993 |
2011 — 2020 | Powell, Craig M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Novel Genetic Models of Autism @ Ut Southwestern Medical Center DESCRIPTION (provided by applicant): Autism spectrum disorders (ASDs) are common, debilitating disorders affecting social interaction, communication, and repetitive behaviors. Recent genetic findings have identified mutations in synaptic cell adhesion genes and genes encoding their interacting protein partners at central synapses as genetic causes of autism spectrum disorders. This proposal will characterize novel and innovative autism mouse models that allow for brain development to take place with a genetic mutation. These particular models allow for reversal of the mutation at various times during brain development and ultimately in specific brain regions. The goal is to narrow the developmental critical period during which such mutations lead to altered brain function and atypical behavior. This information will allow scientists to focus specifically on the time periods and brain regions critical for generation of atypical behavior. In addition, these studies will substantiate feasibility of genetic and certain pharmacological approaches to treatment of a genetic form of autism. Progress to date is substantial in that the genetically reversible mutant mouse models related to autism have been established and characterization has begun. |
0.993 |
2012 — 2015 | Powell, Craig M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Striatal Synaptic Abnormalities in Models of Autism @ Ut Southwestern Medical Center DESCRIPTION (provided by applicant): Autism spectrum disorders (ASDs) are common, debilitating disorders affecting social interaction, communication, and repetitive behaviors. Recent genetic findings have identified mutations in synaptic cell adhesion genes and genes encoding their interacting protein partners at central synapses as genetic causes of autism spectrum disorders. We have created a novel autism model mouse line based on deletion of neuroligin-1. These mice have selective, excessive repetitive behavioral abnormalities of potential relevance to autism. Our preliminary data strongly implicate a decrease in NMDA receptor function in the striatum as a cause of this repetitive behavior phenotype. We now propose experiments to examine the effect of deletion of this gene on cortico-striatal synaptic function in detail. Furthermore, we propose to selectively rescue/treat this phenotype using genetic and pharmacologic approaches. Thus, we will be able to directly connect a specific synapse in a specific brain region due to a specific molecular abnormality with an abnormal behavior, an important basic goal in neuroscience. These experiments will identify novel synaptic and circuit-level mechanisms for obsessive-compulsive disorder- like repetitive behaviors in general. In addition, we hope to identify novel treatment targets for these behaviors for a subset of autistic patients. |
0.993 |
2020 | Powell, Craig M | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular and Cellular Basis of Neurodevelopmental Disorders @ University of Alabama At Birmingham Project Summary/Abstract Neurodevelopmental disorders are common, debilitating disorders including autism, intellectual disability, and perhaps even schizophrenia. Recent genetic findings have identified mutations in multiple genes in various cellular pathways as genetic causes of neurodevelopmental disorders including autism spectrum disorders, intellectual disability, and others. This proposal will characterize novel and innovative genetic mouse models to delineate the function of these genes in the brain. Specifically, the proposal will focus on two genes implicated in either 16p11.2 deletion or autism, both of which are predicted to be involved in overlapping intra- neuronal signaling pathways and regulation of neuronal and synaptic function/development based on preliminary findings. In addition to identifying the neuronal function of these genes in the brain, these studies will identify potential therapeutic strategies for treatment of genetic forms of autism and intellectual disability and possibly other neurodevelopmental disorders. Progress to date is substantial in that two novel mutant mouse models relevant for neurodevelopmental disorders have been established and preliminary characterization of synaptic function, neuronal development, neuronal biochemistry, and neuronal morphology among other aspects of brain function has begun. Unbiased proteomic/transcriptomic approaches to identifying additional, novel downstream targets of these gene products in mammalian brain will generate new hypotheses anticipated to lead to additional potential therapeutic strategies. |
0.931 |