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| EAB and Drugs |
| Tuesday, May 29, 2007 |
| 12:00 PM–12:50 PM |
| Del Mar AB |
| Area: EAB |
| Chair: Ivory Toldson (Southern University) |
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| Navigating the Maze: Using Animal Models of Addiction to Explain Drug Vulnerability in Distressed Communities. |
| Domain: Basic Research |
| IVORY TOLDSON (Howard University), Darryl Neill (Emory University), Young Hoang (Howard University ) |
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| Abstract: Over the past 15 years, animal models of addiction and drug vulnerability have produced compelling evidence that environmental stressors can increase the rewarding effect of drugs, making distressed organisms more prone to drug abuse and dependency. However most animal studies are not easily translated by substance abuse practitioners and policy makers. In this study, authors assessed drug vulnerability among distressed populations by deriving human models from recently published animal models of stress and drug vulnerability. Models were developed through translational analyses and empirically tested using data from the National Survey on Drug Use and Health. Animal variables analyzed included stress procedures, high responders to novelty, social defeat, startle, and sucrose intake, which translated respectively to environmental depravation, risk-taking, social disenfranchisement, anxiety, and anhedonia. Resulting models have implications for future translational research, and drug abuse research, treatment and policy for underserved populations. |
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| Pavlovian Conditioning of Endotoxin Cross-Tolerance in Mice. |
| Domain: Basic Research |
| YUKIKO WASHIO (University of Nevada, Reno), Linda J. Parrott Hayes (University of Nevada, Reno), Kenneth W. Hunter (University of Nevada, Reno) |
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| Abstract: Endotoxin is a biological molecule produced by Gram-negative bacteria (e.g., Escherichia coli) that causes an often fatal syndrome known as septic shock. Endotoxin induces the release of tumor necrosis factor alpha (TNF-a), a cytokine that actually mediates the physiological changes seen in this syndrome. As a defense against overproduction of TNF-a, repeated exposure to endotoxin results in the inhibition of TNF-a release, a phenomenon known as endotoxin tolerance. A method of mimicking endotoxin tolerance could represent a therapeutic approach to this clinical problem. Oberbeck et al. (2003) showed that endotoxin tolerance in rats was subject to elicitation by saccharin when this stimulus was paired with endotoxin in a Pavolvian conditioning arrangement. The present study is a systematic replication of the Oberbeck et al. study with mice. Complete endotoxin tolerance was observed in the conditioning groups, with minimal to no tolerance observed in several different control groups. |
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