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  • Title: Opiate and non-opiate analgesia induced by inescapable tail-shock: effects of dorsolateral funiculus lesions and decerebration.
    Author: Watkins LR, Drugan R, Hyson RL, Moye TB, Ryan SM, Mayer DJ, Maier SF.
    Journal: Brain Res; 1984 Jan 23; 291(2):325-36. PubMed ID: 6697193.
    Abstract:
    Previous studies have demonstrated that inescapable tail-shock can produce either non-opiate or opiate short-term analgesia, dependent on the number of shocks delivered. Additionally, extended exposure to inescapable tail shock can produce long-term, opiate analgesic effects. Several lines of investigation suggest that the psychological dimension of perceived controllability may powerfully influence these phenomena in that each form of opiate analgesia can only be produced following exposure to inescapable, rather than equal amounts and distribution of escapable, shock. This has suggested that these opiate analgesias result from the organism's learning that it has no control over shock. Although it has been assumed that the opiate and non-opiate analgesias induced by tail shock may be subserved by neural circuitry similar to that mediating morphine analgesia and other forms of environmentally induced analgesia, no direct evidence exists to support this assumption. The present study sought to provide an initial attempt at defining the neural circuitry involved in these phenomena by examining the effect of bilateral dorsolateral funiculus (DLF) lesions and decerebration. These experiments revealed that pathways within the spinal cord DLF are critical for the production of short-term non-opiate analgesia, short-term opiate analgesia, and long-term opiate analgesia since bilateral DLF lesions abolished all three pain inhibitory effects. Additionally, it was found that decerebration did not attenuate either the short-term non-opiate or short-term opiate analgesia induced by inescapable tail shock. Combining the observations that these non-opiate and opiate short-term effects are not reduced by decerebration yet are abolished by DLF lesions clearly delimits the source of descending pain inhibition as being within the caudal brainstem.
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