SHOCK-INDUCED HYPERALGESIA IN RATS: DORSOLATERAL FUNICULUS LESIONS UNVEIL HYPERALGESIA AFTER LONG SHOCK. M. W. Meagher *, E. D. Crown, B. Patton, A. R. Ferguson, and J. W. Grau. Dept. of Psychology, Texas A&M Univ., College Station, TX 77843
Exposure to tailshock has a nonmonotonic effect on supraspinally mediated measures of pain reactivity depending on its duration. Brief shock (3, 0.75-s, 1 mA) facilitates vocalization to heat and aversive Pavlovian conditioning, whereas long shock (3, 25-s, 1 mA) inhibits vocalization and aversive conditioning. This inhibitory effect could be mediated by descending systems that inhibit nociceptive transmission in the spinal cord. By removing this source of inhibition we may unveil a hyperalgesic state after long shock. We tested this hypothesis by lesioning the dorsolateral funiculus (DLF), a manipulation that should eliminate descending inhibition while having little effect on the ascending signal.
Experiment 1 examined the effects of DLF lesions on vocalization thresholds and antinociception after exposure to long shock or no shock. DLF lesioned rats vocalized during initial shock exposure and exhibited little antinociception on the tail-flick test after shock. Blocking the antinociception unveiled a powerful hyperalgesia that lowered vocalization thresholds to heat and shock. Experiment 2 evaluated the impact of DLF lesions on fear conditioning after long shock. If DLF lesioned rats are hyperalgesic after long shock, this enhanced pain should increase the affective impact of an aversive unconditioned stimulus (US) and thereby enhance Pavlovian conditioning. After exposure to long shock, rats were transferred to a chamber (CS) where they were exposed to a weak test shock (US). When reexposed to the chamber the next day, greater conditioned freezing was observed in the DLF lesioned rats, indicating that the US was more painful. These findings suggest that neural systems sensitizing pain, and those inhibiting it, are concurrently activated. Removing the inhibitory process revealed a concurrent hyperalgesia. Supported by MH54557 to J.W.G. and M.W.M.
Society for Neuroscience Abstracts, 26 (2000), 653.