Affiliations: | | Cell and Molecular Biology | Tulane University, New Orleans, LA, United States |
Area:
Synaptic Development
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High-probability grants
According to our matching algorithm, Benjamin Hall is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2010 — 2015 |
Hall, Benjamin |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Career: Molecular Regulation of Cortical Synapse Development
Proper brain development involves elaboration of a network containing billions of neurons. This complex process requires the precise initiation, and subsequent maturation, of trillions of synaptic connections between these cells. This research project aims to improve our understanding of the cellular and molecular mechanisms that regulate the developmental maturation of cortical synapse structure and function. These studies focus on the role of a unique neurotransmitter receptor, the n-methyl-d-aspartate (NMDA) receptor. NMDA receptors, which sense glutamate released from other neurons are known to regulate changes in synaptic strength that underlie learning and memory in the adult brain. However, the role of these receptors during synapse development is less well understood. Interestingly, the protein subunit composition of these receptors is tightly controlled during development. NMDA receptors are heteromultimeric structures formed by association of two NR1 and two NR2 subunits. Heightened synaptogenesis, during late embryogenesis and early postnatal life, corresponds with the exclusive expression and incorporation of NR2B subunits to this receptor complex. These studies apply current techniques in genetics, molecular biology and electrophysiology to probe the role of these unique NR2B-containing receptors during a postnatal cortical circuit patterning. Mentorship support is provided for both undergraduate and graduate students. In addition this project aims to promote career opportunities in neuroscience and/or biomedical research to students at minority-serving schools in Louisiana through the initiation of an annual training course in Neurobiology research. This course will be held each spring at the Louisiana Universities Marine Consortium (LUMCON) DeFelice Marine Station in Cocodrie Louisiana.
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1 |
2013 |
Hall, Benjamin |
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. |
Regulation of Protein Translation and Depression by Cortical Nmda Receptors. @ Tulane University of Louisiana
DESCRIPTION (provided by applicant): A single, low dose of the n-methyl d-aspartate receptor (NMDAR) antagonist ketamine produces rapid anti-depressant actions in treatment-resistant depressed patients. This observation strongly supports a role for cortical NMDAR function in depression, which could lead to the generation of new disease models and novel therapeutic strategies. While it is clear that NMDAR antagonism causes a rapid increase in protein translation in cortical neurons, the exact mechanisms underlying these incredible effects remain unclear. One critical unanswered question is how does suppression of NMDAR signaling promote protein translation? NMDARs are heteromultimeric complexes containing two GluN1 subunits and two GluN2 subunits, the latter of which are encoded by four genes (GluN2A-D). Cortical NMDARs are dominated by GluN2A and GluN2B subunits. Recent data have shown that GluN2B-containing NMDARs can act to directly suppress mammalian/mechanistic target of rapamycin (mTOR)-mediated protein translation in cortical neurons, through a cellular signaling mechanism that is uniquely associated with this subunit. Based upon these data, an exciting hypothesis is that relief of GluN2B-mediated suppression of mTOR signaling is responsible for producing the rapid anti- depressant effects observed in response to low dose ketamine treatment. The experiments in this proposal will test this hypothesis with the goal of improving our understanding of the cellular signaling pathways associated with cortical GluN2B-containing NMDARs and determining their involvement in depression.
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1 |