Area:
pain, cannabinoids, neuroinflammation
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, Jenny L. Wilkerson is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2015 — 2017 |
Wilkerson, Jenny Linn |
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. |
Inhibiting Peripheral Diacylglycerol Lipase Beta - a Novel Target For Pain Relief @ Virginia Commonwealth University
DESCRIPTION (provided by applicant): The Identification of novel pharmacological approaches to reduce pain is critical from public health perspective. One of the most common reasons to seek medical attention is that of pain, and collectively pain represents a huge financial burden to society. Once thought to be only mediated solely by neuronal firing, the immune system has been revealed to play a critical role in the regulation, maintenance and transition from acute to chronic pain states. One class that has broad immune relevance during periods of pain is the prostaglandins. Recent discoveries yield insight on a novel pathway of diacylglycerol lipase (DAGL) involvement in the ultimate formation of arachidonic acid, which can then be transformed into prostaglandins. In vitro work shows that inhibiting DAGL-?, one form of DAGL, reduces the biosynthesis of 2-arachidonyl glycerol, the endocannabinoid ligand and a precursor of arachidonic acid. This reduction in free arachidonic acid in turn, results in decreases in the formation of the prostaglandin PGE2 and the pro-inflammatory cytokine tumor necrosis factor- alpha (TNF-?). Therefore, we hypothesize that pharmacological inhibition of DAGL-? with a novel compound, KT109, in mice will lower pro-inflammatory cytokines, prostaglandins and other inflammatory mediators of pain, leading to reversal of behaviors associated with pain. Accordingly, the objectives of this training plan are to characterize the ant-pain effects of DAGL-? inhibitors in murine pain models and determine the underlying in vivo mechanism(s) of action of this class of compounds. The proposed aims to examine these objectives are: 1.) Aim 1: Elucidate the consequences of blocking DAGL- ? in inflammatory pain assays. 2.) Determine the locus of action mediating the pain stimulated and pain depressed behavioral effects of DAGL-? inhibitors in the LPS model of inflammatory pain. 3.) Determine the effects of DAGL-? inhibition on pro-inflammatory and pain mediators. Under these aims the consequences of inhibiting DAGL-? will be investigated in the LPS inflammatory pain model, and the importance of prostaglandins and other pro-inflammatory mediators will be identified. This work aiming to identify a novel mechanism of prostaglandin regulation and subsequent pain control will provide a critical training plan for Dr. Wilkerson to gain the necessary bench skills and conceptual framework to become an independent investigator in developing analgesics that lack abuse potential. Ultimately, the knowledge obtained from this research has the potential to establish DAGL-? as a target linking upstream prostaglandin control to pain relief.
|
1 |