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High-probability grants
According to our matching algorithm, Laurence L. Miller is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2009 — 2010 |
Miller, Laurence L. |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Morphine/Cannabinoid Interactions: Antinociception, Tolerance, and Sensitization @ Univ of North Carolina Chapel Hill
DESCRIPTION (provided by applicant): Agonists of the mu-opioid receptor, such as morphine, are some of the most effective and widely used drugs in the treatment of pain. However, these compounds also have significant effects that limit their therapeutic potential such as the development of tolerance and dependence. One area of interest that has arisen in the search for ways to reduce these unwanted effects involves combining the administration of opioid compounds with drugs that act directly on different systems, but also interact with the opioid system. Ideally, such combinations would enhance the antinociceptive effects of the opioid without increasing unwanted effects. The cannabinoid system interacts with the opioid system and manipulations of cannabinoid signaling may have the potential to be used in this manner. Indeed, cannabinoid agonists have been shown to enhance the antinociceptive effects of opioids such as morphine. However, there is evidence that suggests that cannabinoid/opioid agonist combinations may also produce unwanted effects. For instance, cannabinoid agonists have been shown to enhance the effects of opioids that are associated with their abuse potential. Direct activation of the receptor is not the only way to alter the activity of the cannabinoid system. Recent evidence suggests that altering cannabinoid signaling by manipulating the metabolism and uptake of endogenous cannabinoids, such as anandamide, may hold a therapeutic potential. For intance, altering cannabinoid signaling in this manner produces antinociception, but does not produces some of the unwanted effects associatedwith the administration of cannabinoid agonists. The experiments proposed here build upon these observations by determining whether compounds that inhibit the transport or metabolism of endocannabinoids can enhance the acute antinociceptive effects of morphine (Specific Aim I), and alter the development of tolerance to morphine's antinociceptive effects (Specific Aim II). The experiments described in this proposal will extend existing knowledge regarding the role of the cannabinoid system as a therapeutic target in the treatment of pain. The proposal is also comprised of investigations that are designed to address questions related to the abuse potential of drugs. Findings from these experiments may provide insights that translate to clinical applications.
|
0.988 |
2012 — 2013 |
Miller, Laurence L. |
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. |
Examination of the Functional Consequences of Hiv-1 Tat On Motivated Behavior @ Virginia Commonwealth University
DESCRIPTION (provided by applicant): HIV-1 is associated with a range of neurocognitive deficits referred to as Human Immunodeficiency Virus-Associated Neurocognitive Disorders (HAND) which can have a dramatic impact on patients' lives. The mechanisms underlying these conditions are not entirely known, but there is evidence of HIV-associated neuropathology in brain areas that are consistent with the behavioral deficits associated with HAND. For instance, there is evidence of pathology in the striatum, which is a component of the mesolimbic dopamine system, and has an important role in functions including but not limited to, motor control, learning and memory, and motivation. One potential mediator of the effects outlined above is the HIV protein Tat. Infected glia release Tat and other viral proteins, as well as proinflammatory cytokines. Tat expression has been associated with synapto-dendritic changes in the striatum, neuroinflammation and alterations in the dopamine system in animal models and HIV patients. Research also suggests increased expression of Tat in patients presenting HIV-associated neuropathology. The underlying mechanisms of Tat-induced neuropathology are an active area of research and convergent data suggest a role for toll-like receptors (TLR) such as TLR4. TLR4 gene expression is correlated with neurodegeneration in HIV patients, and Tat and other HIV proteins increase the expression of TLRs. The deficits produced by HAND are ultimately expressed in the behavior of patients. Therefore, a primary goal of the proposed research is to determine the consequences of Tat expression on intracranial self-stimulation (ICSS) using an inducible Tat transgenic mouse model. ICSS is a preclinical behavioral model that is dependent on brain circuitry that is particularly vulnerable t Tat-induced neuropathology. This model is commonly used to explore the mechanisms underlying the abuse-related effects of drugs, and has also been used to examine mechanisms underlying other human disorders that are associated with dysfunction of forebrain dopaminergic circuitry. This proposal aims to adapt ICSS to examine the behavioral effects of the expression of Tat and to correlate effects on this endpoint with the pathology that has been demonstrated in neuroanatomical models. This proposal will also test the hypothesis that Tat-induced neurotoxicity and behavioral impairment can be blocked by treatment with the TLR4 antagonist (+)naloxone. Together, the aims of this proposal are designed to clarify the functional consequences and mechanisms of Tat-induced neurodegeneration and behavioral impairment, and the TLR4 antagonist (+)naloxone will be evaluated as a candidate medication to treat these HIV-related pathologies.
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0.93 |