We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Peter Lipton is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1975 — 1978 |
Lipton, Peter |
N/AActivity Code Description:
No activity code was retrieved: click on the grant title for more information |
Electrical Stimulation On Hippocampal Protein Synthesis @ University of Wisconsin-Madison |
1 |
| 1984 — 1985 |
Lipton, Peter |
N/AActivity Code Description:
No activity code was retrieved: click on the grant title for more information |
Role of Endogenous Adenosine During Anoxia in Hippocampal Slice @ University of Wisconsin-Madison |
1 |
| 1988 — 1991 |
Lipton, Peter |
N/AActivity Code Description:
No activity code was retrieved: click on the grant title for more information |
Ca2+ and Anoxic Damage in the Hippocampal Slice @ University of Wisconsin-Madison
The general problem addressed in this research is the irreversible brain damage resulting from short exposures to anoxia/ischemia. The problem will be studied in a model system, the rate hippocampal slice preparation. Irreversible damage in this system is the permanent blockage of synaptic transmission following 10 minutes oxygen deprivation. The research will address two basic questions about the mechanism of this permanent damage: 1) Is increased cytosolic calcium during anoxia, a major initiator of the damage? and 2) How does glutamate or aspartate release during anoxia contribute to causing the damage? With regard to the last question, the work is designed to test the hypothesis that this amino-acid toxicity during anoxia occurs because of binding to NMA receptors and the subsequent release of calcium from intracellular organelles, probably mediated by increased production of inositol-3-phosphate. The studies address the two questions, and the hypothesis, largely by estimation of changes in cytosolic calcium, made by measurements to tissue regions which are damaged and by correlating damage with changes in calcium and with changes in IP3 in different conditions. Significant advances should be made towards dealing with these two very important issues.
|
1 |
| 1991 — 1995 |
Lipton, Peter |
N/AActivity Code Description:
No activity code was retrieved: click on the grant title for more information |
Role of Glycolysis in Hippocampal Synaptic Transmission @ University of Wisconsin-Madison
Nerve cells can only utilize glucose as an energy source through the process of glucose degradation known as glycolysis. The reason for this metabolic restriction is unknown. In addition to supplying energy to nerve cells, glucose is important for normal synaptic transmission in brain by being a substrate for neurotransmitter synthesis. This research project will examine how the process of glycolysis regulates cerebral synaptic transmission. Dr. Lipton will study whether glycolysis inhibits the formation of ammonia, a compound present in all cells using amino acid derivatives as an energy source. Traces of ammonia have been found to inhibit synaptic transmission. Electrophysiological studies, using hippocampal slices, will be conducted to test whether glucose metabolism is coupled to transmission by supplying energy in the form of ATP and whether glycolysis prevents ammonia build up. Results of this study will elucidate an important aspect of brain metabolism, and the etiology of several nervous system dysfunctions.
|
1 |