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High-probability grants
According to our matching algorithm, Jeffery D. Kocsis is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 |
Kocsis, Jeffery D. |
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. |
Demyelination and Remyelination
The overall objective of this proposal is to investigate mechanisms that underlie abnormal impulse generation and conduction block in demyelinated and remyelinated mammalian axons. An area of emphasis will be on the morphophysiological organization of potassium channels during the course of demyelination and remyelination. The role potassium conductances may have in regulating spike activity will studied for normal, demyelinated, and remyelinated axons. Intrinsic factors such as abnormal membrane properties and extrinsic factors such as axonal "crosstalk" will be analyzed to determine what role they may have in the genesis of abnormal impulse generation in demyelinating lesions. Abnormal impulse generation may contribute to positive signs such as paresthesia or tingling in demyelinating diseases. One hypothesis to be tested in the proposed studies is that increases in spontaneous activity in demyelinating diseases such as multiple sclerosis contributes to activity-dependent excitability depression. The following specific points will be addressed: 1) What role do potassium channels have in regulating spike activity of normal central myelinated axons during the course of normal axon maturation? 2) What is the sequence of change in the effects of potassium channel blocking agents during demyelination and subsequent remyelination of central and peripheral nervous system axons? 3) What changes in action potential characteristics and membrane potential underlie abnormal impulse activity in demyelinated axons? 4) Can axonal "cross-talk" be detected between demyelinated axons, and to what extent do electric field effects versus extracellular potassium ion accumulation contribute to "cross-talk"? 5) Can reducing abnormal impulse activity in demyelinated axons, with the anticonvulsants diphenylhydantoin and carbamazapine, reduce activity-dependent excitability depression and lead to the overcoming of conduction block? Completion of the proposed studies will increase our understanding of the sequence of change in the physiological properties of normal central and peripheral axons during maturation and on how these properties change in response to demyelination and remyelination. The effectiveness of anticonvulsants, on reducing spontaneous activity and allowing for some recovery from activity-dependent excitability depression will be assessed. It will be determined if such modulation of excitability can improve conduction through regions of demyelination.
|
0.97 |
1997 — 2001 |
Kocsis, Jeffery D. |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Cellular and Antiepileptic Drugs On Hippocampal Neurons
Antiepileptic drugs act through a variety of mechanisms to modulate neuronal hyper-excitability. Their pharmacological effects can be mediated by direct interaction with ion channels or receptors, or by alteration in the mode or level of their expression. A key objective of the present study is delineation of acute effects of specific classes of antiepileptics and steroids on hippocampal neurons studied in tissue culture and in brain slice. Somatic conductances (Na+, Ca2+, K+ and GABA-mediated C1- conductances) will be studied using patch clamp techniques on isolated CA1, CA3, and dentate neurons in culture. Intra-dendritic recordings will be obtained in a hippocampal slice preparation to study the actions of antiepileptics on modulating sustained repetitive firing of Na+-mediated dendritic action potentials, GABA-mediated dendritic inhibition and dendritic Ca2+ spikes. We will test the hypothesis that certain antiepileptics exert action on dendritic conductances which are not clearly discernable in somatic recordings. The effects of antiepileptics on the excitability of the nonmyelinated mossy fibers and Schaffer collaterals will be examined to determine if these agents can act by limiting conduction from dentate to CA3 and CA3 to CA1. Putative receptor proteins for steroids are expressed in restricted regions of hippocampus. Do appropriate steroid ligands acutely modulate voltage-gated ion channels or neurotransmitter action in neurons isolated from these regions? High resolution time-lapse video recording and laser confocal microscopy will be used to examine patterns of intracellular Ca2+ levels of hippocampal neurons in culture. Changes in [Ca2+]i will studied following exposure to the excitatory neurotransmitter glutamate. Patterns of change in [Ca2+]i will be compared between soma and dendrite from cells in different regions, and after antiepileptic and steroid application. A key question here is to determine if anti-epileptics, or steroids can effect [Ca+]i by changing intracellular release or uptake. The present studies will focus on antiepileptic drug and steroid action of specific neurons in rat hippocampus studied in both culture and slice. The long-term objective of the proposed studies is to increase our understanding of ion channel organization and Ca2+ signalling in hippocampal neurons and to define the actions of certain anti-epileptics and steroids in modulating neuronal excitability in the hippocampus.
|
1 |
1999 — 2002 |
Kocsis, Jeffery D. |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Cell Transplantation to Repair Demyelinated Spinal Cord
Contusive spinal cord injury often results in demyelination of long tracts, and the prospect of remyelinating these tracts by cell transplantation to achieve a degree of functional recovery is under consideration in man. In this project we propose to study the morphology and electrophysiology of spinal cord axons remyelinated by cell transplantation. The primary demyelinating lesion model will consist of controlled X-irradiation of the lumbar spinal cord followed by intraspinal infections of ethidium bromide; this method produces a reliable demyelinating lesions within the dorsal columns with no endogenous remyelination for 5-6 weeks. After completion of experiments in this model, we will utilize the contusive spinal cord injury model. The following Specific Aims will be addressed: 1) Quantification of Schwann cell remyelination of dorsal column axons: comparison of adult and neonatal cells. 2) Do olfactory ensheathing cells alone, or co-infected with sciatic nerve- derived Schwann cells facilitate remyelination of the EB-X demyelinated spinal cord? 3) Does remyelination induced by induced by transplantation of olfactory ensheathing cells and adult Schwann cells restore electrophysiological function? 4) Does the excitability of primary afferent neurons changes after demyelination and transplant-induced remyelination of the intraspinal processes? 5) Are cell transplantation approaches which are effective for remyelinating chemically-induced demyelinated axons effective in rep airing demyelinated axons in a contusive spinal cord injury model?
|
1 |
2003 — 2007 |
Kocsis, Jeffery D. |
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. |
Marrow Stromal Cell Deliver to Repair the Spinal Cord
[unreadable] DESCRIPTION (provided by applicant): A number of cell types have been used for cell transplantation studies in animal models to remyelinate demyelinated regions of the central nervous. These include committed myelin-forming cells such as oligodendrocytes and Schwann cells as well as precursor cells derived from either embryonic or adult brain. Recently cells within bone marrow have been shown to have the potential to differentiate into myelin-forming cells and to form myelin in animal models of demyelination upon direct injection into the lesion. We have recently shown that intravenous delivery of bone marrow cells can target a chemically-induced demyelination site in the rat spinal cord and remyelinate these axons. This opens the intriguing prospect of delivery of cells to systemically target sites of demyelination and to achieve myelin repair. The precise cell type within this fraction of bone marrow is not known, nor is the full repair potential of this approach understood. In this proposal we will study isolated bone marrow stromal cells (MSCs) to quantify remyelination induced by direct intraspinal and intravenous delivery of the MSCs to determine the extent to which we can repair a demyelinated lesion. These results will be compared to similar studies on injection of bone marrow mononuclear cells. We will use both anatomical and electrophysiological techniques to study the functional recovery of the remyelinated axons. We will also use a second lesion model system (a myelin-deficient mouse, shiverer) to determine if myelin repair by systemic bone marrow delivery can be achieved in a naturally occurring model of dysmyelination where gliosis is present. Many of the myelin profiles observed subsequent to bone marrow transplantation are characteristic of peripheral myelin. We will distinguish central from peripheral myelin. Completion of these studies should allow us to better understand the potential of MSCs to repair myelin. While these approaches are experimental in animal models, the prospect of using an expandable and renewable source of cells from bone marrow to repair the demyelinated CNS by systemic delivery has implications for future consideration of such an approach in man. [unreadable] [unreadable]
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1 |