Area:
Toxicology, Neuroscience Biology
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High-probability grants
According to our matching algorithm, Gail D. Zeevalk is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 — 1986 |
Zeevalk, Gail D |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Cytotoxicity in Isolated Retinal Neurons @ Rutgers the St Univ of Nj New Brunswick |
0.969 |
1995 — 1997 |
Zeevalk, Gail 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. |
Retinal Metabolism and Neurotoxic Mechanisms @ Univ of Med/Dent Nj-R W Johnson Med Sch
DESCRIPTION (Adapted from applicant's abstract): Retinal ischemia, caused by one of several retinal vascular disorders, can result in vision impairment and blindness. The overall aim of the laboratory is to delineate the cellular mechanisms involved in retinal neurodegeneration and in particular, to elaborate the role played by glutamate and NMDA receptors in the neurodegeneration associated with metabolic stress encountered in conditions of retinal ischemia, hypoxia and hypoglycemia. The current application is an extension of past efforts and is designed to understand the early cellular events that occur during inhibition of retinal cellular metabolism which lead to irreversible cell death. Studies will utilize an ex vivo chick retinal preparation which we have used extensively in prior work. Aim 1 will determine the contribution of acute cellular swelling induced by metabolic stress or direct glutamate receptor overstimulation to irreversible delayed cell death. Acute cell swelling is a rapid consequence of both ischemia and acute excitotoxicity. Previous studies with the retinal model have shown an intimate link between inhibition of energy metabolism and activation of excitotoxic processes initially involving the NMDA subtype of glutamate receptor. The current studies will test the hypothesis that, in retina, metabolic stress or excitatory amino acid (EAA) induced acute cell swelling is caused by reversal of the GABA transporter and that this swelling contributes to delayed cell death. Aim 2 will examine the contribution of glial metabolism to NMDA receptor mediated damage due to metabolic stress. Studies will test the hypothesis that metabolic stress in the Muller cells contributes to neuronal damage. The extent to which glial metabolism will selectively be inhibited with fluorocitrate or fluoroacetate and the effect on neurons evaluated. Additionally, glial metabolism will be inhibited during an EAA challenge or general mild metabolic stress to determine if inhibition of glial metabolism potentiates neuronal damage. Aim 3 will examine the role of endothelin (ET) in retina and in mediation of damage due to metabolic stress. The location of ET in retina will be determined. Signal transduction mechanisms linked to ET's action in retina will be examined and include activation of Ca2+ channels, protein kinase C and regulation of cAMP and cGMP. The effect of ET on neurotransmitter release and on modulation of metabolic stress induced damage in retina will be investigated. Overall, these studies are expected to expand upon previous findings to develop a more detailed knowledge of the cellular mechanisms underlying retinal cell damage due to metabolic stress. An understanding of such mechanisms may lead to future strategies to prevent damage due to retinal ischemia.
|
0.904 |
1998 — 2008 |
Zeevalk, Gail 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. |
Energy Metabolism, Dopamine Neurons and Neurotoxicity @ Univ of Med/Dent Nj-R W Johnson Med Sch
DESCRIPTION: Defects in energy metabolism have been reported in patients with Parkinson's disease (PD), thus implicating disturbances in energy metabolism as a part of the etiology. Although the presence of an energy impairment in PD is not at present identified as a primary event, it is clear that it is present at a time when dopamine neurons are declining in the PD patient. Thus, it is important to understand how metabolic stress affects DA neurons. This study will examine energy stress induced by inhibition of succinate dehydrogenase with malonate or 3-nitroproprionic acid, on DA neurons focusing on 2 areas of potential cellular mediators of the damage, i.e. glutamate receptor overstimulation and oxidative stress. in vivo (rat) and in vitro (rat mesencephalic cultures) will be used for the studies. It is hypothesized that mild metabolic stress reduces energy status (ATP/ADP), decreases Na+/K+ ATPase activity, degrades the membrane potential, which results in glutamate receptor overstimulation, generation of reactive oxygen species and an ensuing oxidative stress. Studies in aim 1 will use in vitro and in vivo approaches to temporally examine ATP/ADP status, Na+/K+ ATPase inhibition and changes in membrane potential in relationship to toxicity during energy stress induced damage. The sensitivity of DA neurons to excitotoxins and the involvement of glutamate receptors in energy stress induced damage will also be explored. Overstimulation of glutamate receptors is postulated to be a link between mild metabolic stress and generation of an oxidative stress. in vivo and in vitro studies in sub aims of 1 and 2 will temporally examine oxidized/reduced glutathione status, protein thiol loss, protein-glutathione mixed disulfide formation and lipid peroxidative damage to provide evidence of an oxidative component to toxicity due either to excitotoxicity or metabolic inhibition. The ability of spin trap agents to protect vs excitotoxicity or damage to DA neurons due to a metabolic stress will provide additional evidence of oxidative stress. It is further hypothesized that DA neurones as compared with other neuronal populations are more susceptible to a mild impairment of energy metabolism because of the intrinsic oxidative stress placed on them due to DA metabolism and oxidation. The vulnerability o DA neurons will be compared both in vivo and in vitro with the GABA population since this is a major neurotransmitter population found in the striatum and substantia nigra. In sub aims of 1 and 2, we will examine the importance of the antioxidant systems glutathione and catalase in protecting DA or GABA neurons during impaired energy metabolism by manipulating these systems to either inhibit, enhance or deplete them. The role of DA metabolism by MAO or DA oxidation will also be addressed in vivo and in vitro to determine if these events contribute to the relative vulnerability of DA neurons to energy stress. These studies will provide important information regarding the cellular mechanisms mediating damage to DA neurons to energy impairment and the possible reasons for their unique sensitivity and will provide insight into the ongoing loss of the neurons in PD.
|
0.904 |