Area:
Pharmacology, Toxicology, Neuroscience Biology
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High-probability grants
According to our matching algorithm, Robert F. Halliwell is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2004 — 2006 |
Halliwell, Robert F |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
A Study of Nsaids On Neuronal Ion Channels @ University of the Pacific-Stockton
DESCRIPTION (provided by applicant): Non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely used medicines worldwide and a common source of self-poisoning. These agents rapidly enter the Central Nervous System (CNS) and recent work has shown that they can delay the onset and slow the progression of Alzheimer's Disease. Several NSAIDs are also analgesic even when administered directly into the CNS and fenamate NSAIDs have anti-epileptic and neuroprotective properties. Despite these findings, little is known of the effects of these drugs on neuronal function. Recent experiments by the applicant have begun to address the hypothesis that NSAIDs modulate neuronal receptors and ion channels. Our initial experiments have concentrated on the effects of fenamate NSAIDs on GABA-A receptors. We have demonstrated that mefenamic acid modulates GABA-A receptors in the low therapeutic dose range and that such actions are highly receptor subtype selective. These data are important since they are the first to indicate that NSAIDs may have effects on synaptic transmission and suggest that such actions might contribute significantly to their clinical effects. These results also suggest that fenamates represent a new class of GABA-A receptor modulator with new but unrecognized therapeutic uses. The aims of this study are, therefore, to address the hypothesis that NSAIDs have effects on neuronal function. This project will focus on the interaction between fenamate NSAIDs and central neuronal ligand- and voltage-gated ion channels. We will utilize single cell electrophysiological and cell culture techniques, firstly, to determine the molecular mechanism of action of fenamates on hippocampal neuron GABA-A receptors. Secondly we will further characterize the complex actions of fenamates on recombinant human GABA-A receptors. Thirdly, we will determine the selectivity of action of fenamates on neuronal function by determining their effects on several other native ligand- and voltage-gated ion channels. These experiments will contribute to our understanding of the molecular mechanisms by which NSAIDs produce their diverse central effects. These data may also provide new drug leads and/or novel molecular targets for the treatment of pain and/or neurodegenerative diseases such as Alzheimer's type dementias.
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