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High-probability grants
According to our matching algorithm, Bryan W. Luikart is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2006 — 2008 |
Luikart, Bryan W |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
The Integration of New Neurons Into the Adult Dentate Gyrus @ Oregon Health and Science University
[unreadable] DESCRIPTION (provided by applicant): New neurons are continually born and are incorporated into the mature circuitry of the adult central nervous system. The hippocampal dentate gyrus is a brain region where there is a substantial level of neurogenesis in adult birds and mammals. This brain region is important for encoding new memories. Increased hippocampal neurogenesis has been correlated with enhanced learning. Enhanced neurogenesis is elicited by exercise and antidepressant medications - treatments that are known to be important for enhancing mood in depressed patients. The ability to generate new neurons is unique to two regions in the central nervous system. Further, it is the lack of this ability throughout most central nervous system regions that results in a poor ability to recover from brain injuries and neurodegenerative disorders. While much work has focused on the birth of new neurons in the hippocampal brain region there has been less emphasis on the mechanisms by which new neurons survive and integrate into the mature synaptic circuitry. It is known that neural activity can enhance the integration of newborn neurons into the dentate gyrus. In aim 1 we propose to examine the mechanisms by which activity influences the integration and survival of newborn neurons in the adult central nervous system. Specifically we will use brain slices from animals expressing a genetically encoded marker of newborn neurons and examine how stimulation affects growth, synapse formation, and synapse function of newborn neurons. We will use live-imaging methods to measure growth and synapse formation and electrophysiological recordings to measure synapse formation and function. In aim 2 we propose to study the molecular mechanisms important for integration. We can target newborn neurons for genetic modification by injecting molecularly engineered viruses into the brains of live mice. With this approach we can knockdown genes that we hypothesize to be important for integration and examine the effect genetic manipulation on the growth and synapse formation of the newborn neurons. The results of the proposed experiments will expand our knowledge about how activity and genetic expression influence the ability of newborn neurons to survive in the adult central nervous system. An understanding of how new neurons integrate into mature synaptic circuitry is fundamental to our understanding of the brain. I believe that this knowledge will be important to develop therapies to enhance cognitive abilities in the learning impaired, mood in depressed patients, and functionally replace damaged neurons in patients with acquired brain injuries or neurodegenerative disorders. [unreadable] [unreadable]
|
0.907 |
2012 — 2019 |
Luikart, Bryan W |
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. |
The Impact of Pten Signaling On Neuronal Form and Function
DESCRIPTION (provided by applicant): Autism Spectrum Disorder (ASD) is a developmental disorder characterized by inappropriate responses to social and sensory stimulation, restricted communication, and stereotyped behavior. Heterozygous mutations in the gene Pten (phosphatase and tensin homolog on chromosome 10) have been identified in 5 to 17% of patients presenting with autism and macrocephaly. Further, experimental deletion of Pten in the mouse brain also causes macrocephaly and deficits in social behavior, suggesting a causative role for Pten dysfunction in the development of ASD. At the cellular level, Pten knockdown results in aberrant growth and increased excitatory synaptic function. Thus, study of Pten fits perfectly with our long-term goal of understanding how synaptic connectivity and activity contribute to complicated cognitive and emotional functions. Our central hypothesis is that Pten dysfunction in autism patients results in aberrant excitation of susceptible neural circuits. Guided by this hypothesis, the specific aims of this proposal will strengthen our understanding of the molecular and neurophysiological basis of ASD. Manipulation of Pten in vivo presents a unique opportunity to examine the neurophysiological basis of autism in a model organism. Our first aim will test the hypothesis that Pten knockdown results in hyperexcitability of a defined circuit. The symptoms of autism are often most severe during development, and decrease in severity during adolescence and adulthood. Identification of endogenous mechanisms by which the adult brain becomes more resistant to genetic insults causing autism could lead to new treatments. Our second aim will test the hypothesis that developing neurons are intrinsically more sensitive to the effects of Pten knockdown. A key gap in our understanding of how Pten contributes to autism exists because we have not examined whether Pten point mutations are equivalent to knockdown. Examining point mutations found in patients will serve as a starting point to identify intra- and intermolecular interactions of Pten relevant to the autism phenotype. For the third aim, we will test the hypothesis that point mutations identified in patients will reslt in cellular phenotypes relevant to the autism model. This proposal will use the innovative approaches of viral-based knockdown and molecular substitution in vivo, coupled with detailed morphological and electrophysiological analyses. The broad goal of this research is to define the molecular and physiological basis of how Pten dysfunction contributes to some forms of autism. PUBLIC HEALTH RELEVANCE: This research proposal is relevant to public health because it addresses issues related to the molecular pathophysiology of autism spectrum disorder. Thus it is directly relevant to the part of NIH's mission outlined in PA-10-158 - Research on Autism and Autism Spectrum Disorders.
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0.954 |