Affiliations: | | The Center for Neuropharmacology & Neuroscience | Albany Medical College, Albany, NY, United States |
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High-probability grants
According to our matching algorithm, Mark Fleck is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2001 — 2004 |
Fleck, Mark W |
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. |
Agonist Gating of Non-Desensitizing Ampa Receptors
DESCRIPTION: AMPA-type glutamate receptors are expressed throughout the mammalian central nervous system and represent the principal means of fast excitatory signaling at central synapses. Functional AMPA receptors are homo- or hetero-oligomeric complexes generated by assembly of four individual subunits, GIuRI -4, each of which exists in at least two alternatively spliced isoforms. The molecular diversity that arises from varying subunit and splice-variant composition imparts unique functional properties to the receptors that can differ in their ionic permeabilities, unitary conductances, ligand binding affinities, and kinetics of activation, deactivation, desensitization, and recovery from desensitization. All of these properties are important to synaptic signaling. Particularly intriguing is the very rapid desensitization of AMPA receptor currents within a few milliseconds upon exposure to glutamate. The impact of such rapid desensitization on the synaptic response is yet unresolved, however the recent description of several non-desensitizing AMPA receptor mutants presents a unique opportunity to study how desensitization controls receptor and synaptic function. The proposed studies will compare the functional properties of the fast-desensitizing wild type and non-desensitizing mutant AMPA receptors by whole-cell and outside-out patch clamp recording in conjunction with ultra fast solution exchange techniques. Experiments will seek to determine the extent to which desensitization governs the receptor affinity for peak activation by glutamate and the rate of deactivation following removal of glutamate. These properties in turn limit the magnitude and duration of the postsynaptic response. Studies will also examine the mechanism of allosteric drug actions that target desensitization and seek to elucidate some of the amino acid residues that are important for desensitization. Results of these investigations should facilitate our understanding of the functional and pharmacological properties of AMPA receptors, their regulation by subunit composition, and the structural elements that are involved in this regulation.
|
0.958 |
2001 |
Fleck, Mark |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Biosensor Patch Detection of Quantal Glutamate Release @ Albany Medical College of Union University
008007 Fleck
Cell-cell signaling in the nervous system involves the regulated release of chemical neurotransmitters at specialized synaptic contacts. The principal excitatory neurotransmitter in the mammalian brain is glutamate. Yet the methods available to measure glutamate are indirect and insufficient to study its release in real time or at individual release sites. This proposal seeks to develop a reliable, quantitative, and direct method to measure the release of glutamate during synaptic transmission. Highly selective glutamate sensitive proteins will be employed that generate a measurable current upon glutamate binding. The proteins have been cloned, genetically engineered to enhance their fidelity of signal transduction, and will be incorporated into a biosensor probe. Studies are proposed to test the spatial and temporal limits of detection by such probes while measuring the variability of 'quantal' packets of glutamate, perhaps a few thousand molecules, as they are released during synaptic activity. If successful, these studies will provide a means to address previously intractable questions of synaptic physiology. Glutamate release is broadly involved in nervous system function and is highly regulated. Developmental and use-dependent changes in the strength of glutamate transmission are important for synapse maturation, learning and memory. Dysregulation of glutamate transmission is implicated in cognitive-memory impairments, epilepsy, affective disorders, and neurodegenerative disease. Therefore, it is important to advance our understanding of the process and regulation of glutamate release.
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1 |