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Full-Text Articles in Medicine and Health Sciences

Glial Cell Modulators And Associated Anti-Inflammatory Activity: Implications In Reducing Methamphetamine Abuse-Related Behaviors In Rodents, Sarah Snider Apr 2014

Glial Cell Modulators And Associated Anti-Inflammatory Activity: Implications In Reducing Methamphetamine Abuse-Related Behaviors In Rodents, Sarah Snider

Theses and Dissertations

Methamphetamine is a psychomotor stimulant that produces hyperactivity and euphoria and can lead to drug-seeking and abuse. An estimate from 2005 put the cost of methamphetamine abuse to society at an estimated 23.4 billion dollars. One of methamphetamine's effects is activation of glial cells and associated neuroinflammatory activity in the periphery and CNS. Glia are responsible for maintaining calcium homeostasis, neuroplasticity, immune activity, and cell signaling. Activation of glia and neuroinflammation are becoming recognized as links in drug abuse-related behavior. The goal of the present work was to assess the ability of ibudilast, AV1013, and minocycline, three glial cell modulating …


Effect Of Cannabinoids On Pain-Stimulated And Pain-Depressed Behavior In Rats, Andrew Kwilasz May 2013

Effect Of Cannabinoids On Pain-Stimulated And Pain-Depressed Behavior In Rats, Andrew Kwilasz

Theses and Dissertations

Cannabinoids produce antinociception in many preclinical models of acute and chronic pain. In contrast, cannabinoids produce inconsistent analgesia in humans, showing little or no efficacy in treating acute pain, with modest efficacy in treating chronic inflammatory pain. This discrepancy may reflect an overreliance on preclinical assays of pain-stimulated behaviors, defined as behaviors that increase in rate or intensity following delivery of a noxious stimulus. In these assays, antinociception is indicated by a reduction in pain-stimulated behaviors, and antinociception is produced either by a reduction in sensory sensitivity to the noxious stimulus (i.e. true analgesia) or by false positive motor impairment. …


Activation Of Peroxisome Proliferator-Activated Receptor G In Brain Inhibits Inflammatory Pain, Dorsal Horn Expression Of Fos, And Local Edema, Jenny Morgenweck, Omar D. Abdel-Aleem, Katelyn C. Mcnamara, Renee R. Donahue, M Z. Badr, Bradley K. Taylor Jan 2010

Activation Of Peroxisome Proliferator-Activated Receptor G In Brain Inhibits Inflammatory Pain, Dorsal Horn Expression Of Fos, And Local Edema, Jenny Morgenweck, Omar D. Abdel-Aleem, Katelyn C. Mcnamara, Renee R. Donahue, M Z. Badr, Bradley K. Taylor

Renee R. Donahue

Systemic administration of thiazolidinediones reduces peripheral inflammation in vivo, presumablybyacting at peroxisome proliferator-activated receptor g (PPARg) in peripheral tissues. Based on a rapidly growing body of literature indicating the CNS as a functional target of PPARg actions, we postulated that brain PPARg modulates peripheral edema and the processing of inflammatory pain signals in the dorsal horn of the spinal cord. To test this in the plantar carrageenan model of inflammatory pain, we measured paw edema, heat hyperalgesia, and dorsal horn expression of the immediate-early gene c-fos after intracerebroventricular (ICV) administration of PPARg ligands or vehicle. We found that ICV rosiglitazone …


Ranolazine Attenuates Behavioral Signs Of Neuropathic Pain, Harry J. Gould Iii, Colleen J. Garrett, Renee R. Donahue, Dennis Paul, Ivan Diamond, Bradley K. Taylor Jan 2009

Ranolazine Attenuates Behavioral Signs Of Neuropathic Pain, Harry J. Gould Iii, Colleen J. Garrett, Renee R. Donahue, Dennis Paul, Ivan Diamond, Bradley K. Taylor

Renee R. Donahue

Ranolazine modulates the cardiac voltage-gated sodium channel (NaV 1.5) and is approved by the FDA in the treatment of ischemic heart disease. Ranolazine also targets neuronal (NaV 1.7, 1.8) isoforms that are implicated in neuropathic pain. Therefore, we determined the analgesic efficacy of ranolazine in a preclinical animal model of neuropathic pain. Both intraperitoneal and oral administration of ranolazine dose-dependently inhibited the mechanical and cold allodynia associated with spared nerve injury, without producing ataxia or other behavioral side effects. These data warrant clinical investigation of the potential use of ranolazine in the treatment of neuropathic pain.