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High-probability grants
According to our matching algorithm, Peter Shrager is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1987 — 2004 |
Shrager, Peter G |
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. |
Neuron-Neuroglia Interactions @ University of Rochester
DESCRIPTION (provided by applicant): Neurons are highly polarized cells and require the sequestration of ion channels, as well another components, in specific locations. Within myelinated axons, voltage -dependant Na+ channels are clustered and anchored at initial segments and nodes of Ranvier, and this organization is essential for both the integration of information and the rapid propagation of action potentials overlong distances. The project seeks to understand the mechanisms involved in achieving and maintaining this distribution. This work is important both during development of the nervous system, and also in several disease states, including multiple sclerosis and Guillain-Barre Syndrome. This research seeks first to distinguish between two very different hypotheses for the neuron-glial interactions that are responsible for Na+ channel clustering. Are sites of high channel density determined solely by the axon, or are they induced by myelinating glia? Further, is a destabilization of the cytoskeleton the immediate cause of Na+ channel diffusion to these sites? We have recently found that contactin, a surface protein with homology to one of the auxiliary subunits of the Na+ channel, can increase expression of this channel several-fold in-transfected cells. We seek now to characterize the molecular basis for this regulation, and to investigate the function of contactin in neurons and glia. This will be done through mutational analysis, biochemical association assays, and functional measurements. The ultimate aim is to understand how critical neuronal components are regulated and distributed to insure reliable signaling. This information will then be helpful in designing therapies for diseases of the brain, spinal cord, and periphery.
|
0.958 |
1994 — 2000 |
Shrager, Peter G |
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. |
Neuron/Neuroglia Interactions @ University of Rochester
The correlation between pathology and neurological function in multiple sclerosis and other demyelinating diseases is poor, and the event responsible for the initial loss of neural function is unknown. This project seeks to investigate fundamental aspects of signal transmission in nerve fibers that have been altered by chemical or autoimmune mechanisms designed to reproduce the conduction failure seen in these diseases. This approach will allow an evaluation of the relation of immune reactions and structural changes to electrophysiological events. Using both optical techniques with voltage-identified single axons during all stages of demyelination and recovery. The immune properties of axons following their close association with T lymphocytes and macrophages. The possible involvement of cytokines and antibodies with ionic channels and with conduction will likewise be tested. During repetitive stimulation myelinated axons possess both refractory and hyper-excitable periods. In demyelinated fibers, with reduced safety factors, these phenomena are altered and lead to an axonal "coding" of action potential patterns. The mechanisms responsible for this process will be investigated by following signals optically at several sites along an identified fiber. Ionic channels in the internodal axon membrane, which may be silent in normal function, incur considerable importance with demyelination, especially with respect to recovery of propagation. These channels will be characterized by single channel patch clamp analysis, and their control by pharmacological means explored. The restoration of function following demyelination depends upon glial association as well as on ionic channels, and it remains unclear how remission can occur in multiple sclerosis since remyelination in the central nervous system is rare and incomplete. Conduction in mammalian axons that have been demyelinated by autoimmune procedures will be followed optically in order to determine the minimum requirements for recovery. The experiments in this proposal will be performed both on peripheral fibers in the adult sciatic nerve, and in the central nervous system through the use of organotypic explant cultures and acute brain slices. Possible means of intervening in various steps of the disease process will be explored.
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0.958 |