Neuroscience 2001 Abstract
| Presentation Number: | 509.17 |
|---|---|
| Abstract Title: | Differential effects of intracerebroventricular naltrexone and specific opiate receptor subtype antagonists on formalin- and illness-induced hyperalgesias. |
| Authors: |
Wiertelak, E. P.*1
; Koski, D.1
; Hoffert, D.1
; Connors, E.1
; Hicks, K.1
1Dept Psychol, Macalester Col, St. Paul, MN |
| Primary Theme and Topics |
Sensory Systems - Pain Modulation -- Opiods, cannabinoids and other peptides and receptors |
| Session: |
509. Pain modulation: descending control Poster |
| Presentation Time: | Tuesday, November 13, 2001 8:00 AM-9:00 AM |
| Location: | Exhibit Hall V-1 |
| Keywords: | opioid, pain modulation, conditioning |
We have previously reported (EPW, SFN Abstract, 1996, 97, 99) evidence for a spinal opiate mechanism in the hyperalgesic state (tailflick test) that results from the intraperitoneal administration of lipopolysaccharides (LPS; pyretic) or lithium chloride (LiCl; emetic), through the pairing of a unique flavor with illness, i.e., conditioned hyperalgesia, and the subcutaneous injection of formalin (dorsum of hindpaw). The goal of the present experiments was to examine supraspinal opiate involvement in LiCl- and formalin -induced hyperalgesias in rats previously implanted (one to two weeks earlier, to allow for recovery) with intracerebroventricular (ICV) cannulae (3rd ventricle).
Here, the ability of ICV injection of specific opiate antagonists (CTOP, Naltrindole, Nor-Binaltorphimine) and naltrexone to dose-dependently block LiCl- and formalin-induced hyperalgesias in the tailflick test was compared to ICV vehicle controls. In contrast to vehicle controls, ICV injections of naltrexone (10, 1.0, and 0.1 ug) blocked the illness-induced hyperalgesia resulting from LiCl; ICV specific antagonists produced differential effects. Similarly, formalin hyperalgesia also was antagonized by naltrexone; specific antagonist experiments for formalin hyperalgesia are ongoing. To date, the results suggest differing roles for supraspinal mu, delta, and kappa opiate receptors in the mediation of formalin- and LiCl-induced hyperalgesias.
Here, the ability of ICV injection of specific opiate antagonists (CTOP, Naltrindole, Nor-Binaltorphimine) and naltrexone to dose-dependently block LiCl- and formalin-induced hyperalgesias in the tailflick test was compared to ICV vehicle controls. In contrast to vehicle controls, ICV injections of naltrexone (10, 1.0, and 0.1 ug) blocked the illness-induced hyperalgesia resulting from LiCl; ICV specific antagonists produced differential effects. Similarly, formalin hyperalgesia also was antagonized by naltrexone; specific antagonist experiments for formalin hyperalgesia are ongoing. To date, the results suggest differing roles for supraspinal mu, delta, and kappa opiate receptors in the mediation of formalin- and LiCl-induced hyperalgesias.
Supported by Grant DA09289 from the National Institute on Drug Abuse at the National Institutes of Health (to EPW).
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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