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High-probability grants
According to our matching algorithm, Peter C. Ruben is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1991 — 2006 |
Ruben, Peter C |
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. |
Slow Inactivation of Sodium Channels @ University of Hawaii At Manoa
The broad, long-term objectives of this proposal are to (1) characterize the structure-function relationship of the parts of sodium channels that control slow inactivation and to (2) assess the potential contribution of sodium channel slow inactivation in the mechanisms of epilepsy. The Specific Aims are: 1) to measure the properties of sodium channels during slow inactivation and to measure the voltage sensitivity and kinetics of slow inactivation, 2) to express channels with mutations of the S4 region of repeats M and IV to determine whether that part of the sodium channel molecule controls slow inactivation, and 3) to determine the differences between the F(Vh) curves measured from normal neurons and neurons from spontaneously epileptic (tottering) mice, and to identify anti-epileptic agents that affect the voltage dependence and kinetics of slow inactivation. The health-relatedness of this proposal is its application to epilepsy; a critical factor in neuronal hyperexcitability (that could lead to epilepsy) is a right-shift in the midpoint of the F(Vh) curve which leads to an increase in the number of channels available for activation from resting potential. The kinetics, effective valence, and voltage dependence of the F(Vh) curve in crayfish giant axons will be measured using axial-wire voltage clamp. The effects of anti-epileptic drugs such as diphenyl- hydantoin, carbamasepine and sodium valporate on properties of the F(Vh) curve in crayfish will be studied. Native and mutated sodium channels will be expressed in Xenopus oocytes, and macroscopic currents will be recorded using two-electrode voltage clamp and outside-out patch configuration. Slow inactivation properties will be compared between wild-type channels and those with S4, repeats III and/or IV amino acid replacement and deletion mutations produced by site-directed mutagenesis. Properties controlling slow inactivation will be compared between neurons cultured from non-phenotypic tottering (spontaneously epileptic) mice using patch clamp techniques.
|
0.948 |
| 2002 — 2003 |
Ruben, Peter C |
F33Activity Code Description:
To provide opportunities for experienced scientists to make major changes in the direction of research careers, to broaden scientific background, to acquire new research capabilities, to enlarge command of an allied research field, or to take time from regular professional responsibilities for the purpose of increasing capabilities to engage in health-related research. |
The Role of Sodium Channels in Neocortical Dendrites
DESCRIPTION (provided by applicant): The specific aims of the proposed research are to investigate the role of voltagegated sodium channels in back-propagation of action potentials in the dendrites of neocortical cells. Specifically, we will determine whether modulation of slow inactivation in sodium channels is responsible for an increase in sodium channel availability that underlies back propagation of action potentials into dendrites. The hypotheses we will test are that (1) an increase in sodium channel availability is the basis for dendritic electrogenesis in response to high frequency discharges, and (2) modulation of sodium channels by cell signaling pathways is responsible for an decrease in steady-state probability of slow inactivation which leads to increased channel availability. The health-relatedness of the proposed research is that back propagation is an important regulator of synaptic efficacy. Understanding the biophysical basis for back propagation will help researchers understand the physiological mechanisms of learning and memory.
|
0.964 |