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High-probability grants
According to our matching algorithm, Patric K. Stanton is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2008 — 2012 |
Stanton, Patric K. |
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. R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Presynaptic Long-Term Synaptic Depression @ New York Medical College
Long-lasting activity-dependent alterations in the strength of synaptic connections are thought to be essential substrates of memory. Long-term potentiation (LTP) of synaptic transmission has been heavily studied, long-term depression (LTD) of synapse strength much less so. Prolonged low-frequency synaptic stimulation elicits robust LTD of synaptic strength. Our previous studies suggest that LTD consists of multiple, distinct cascades, one dependent on the actions of the intercellular messenger nitric oxide (NO), production of cyclic GMP and inhibition of cyclic AMP-dependent protein kinase, which acts on presynaptic terminals to persistently reduce transmitter release. Induction of presynaptic LTD can depend on activation of N-methyl-D-aspartate receptors (NMDAR), or on co-activation of group I and II metabotropic glutamate receptors. Using two-photon laser scanning microscopy of FM1-43 release from hippocampal synaptic terminals, we have shown that NMDAR-dependent presynaptic LTD is associated with a selective reduction in release from the rapidly-recycling vesicle pool (RRP). In this renewal application, we propose studies that employ electrophysiological recording and two-photon confocal fluorescence imaging techniques in in vitro hippocampal slices to answer the following questions: (1) Are NMDAR-dependent and mGLuR-dependent forms of LTD induced by different biochemical pathways? (2) What are the effects of NMDAR- and mGluR-dependent forms of LTD on kiss-and-run[unreadable] release, vesicle recycling and pool exchange rates visualized with FM1-43 and in synaptopHluorin-expressing mice?, and 3) What is the role of G[unreadable]? binding the synaptic vesicle proteins or voltage-dependent calcium channels in presynaptic terminals in NMDAR- versus mGluR-dependent LTD? There is a probable role for LTD in memory processing, and impairments in LTD may contribute to pathologies of memory storage such as Alzheimer[unreadable]s Disease. LTD-like dampening of neuronal excitation could be important in preventing epileptic seizures and reducing excitotoxic neuronal injury. The long-term regulation of transmitter release has far-reaching importance to normal synaptic processing dynamics, and controlling pathologic glutamate release during injury or disease.
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