Glutamate is the major excitatory neurotransmitter in the brain. The amount of glutamate transported into vesicles could change the strength of a synapse. This proposal aims to 1) distinguish between competing models of vesicle filling by asking whether glutamate transport is necessary for increases in vesicle size, 2) determine the number of glutamate transporters on a vesicle, and 3) investigate homeostatic mechanisms that attenuate the excitatory effects of excess glutamate release. Understanding the consequences of reduced and increased vesicular glutamate transporter expression and their effects on synapse strength will provide insight into the biology of glutamatergic synaptic vesicles, excess glutamate release and excitotoxicity, and homeostatic mechanisms that regulate glutamate release. ? ?

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31NS054467-01
Application #
7054854
Study Section
Special Emphasis Panel (ZRG1-F03B (20))
Program Officer
Porter, John D
Project Start
2006-02-01
Project End
2008-01-31
Budget Start
2006-02-01
Budget End
2007-01-31
Support Year
1
Fiscal Year
2006
Total Cost
$26,773
Indirect Cost
Name
Washington University
Department
Neurosciences
Type
Schools of Medicine
DUNS #
068552207
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Daniels, Richard W; Miller, Bradley R; DiAntonio, Aaron (2011) Increased vesicular glutamate transporter expression causes excitotoxic neurodegeneration. Neurobiol Dis 41:415-20
Daniels, Richard W; Gelfand, Maria V; Collins, Catherine A et al. (2008) Visualizing glutamatergic cell bodies and synapses in Drosophila larval and adult CNS. J Comp Neurol 508:131-52
Wu, Chunlai; Daniels, Richard W; DiAntonio, Aaron (2007) DFsn collaborates with Highwire to down-regulate the Wallenda/DLK kinase and restrain synaptic terminal growth. Neural Dev 2:16