Spinal and Peripheral μ Opioids and the Development of Secondary Tactile Allodynia After Thermal Injury

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Abstract

Local thermal injury to the paw leads to an increased sensitivity to a noxious stimulus applied to the site (primary thermal hyperalgesia) and an increased sensitivity to tactile stimuli in skin sites adjacent to the primary injury (secondary tactile allodynia; 2°TA). We sought to define the peripheral and spinal actions of μ opioids in regulating 2°TA. First, a mild thermal injury was induced on one heel, producing 2°TA. This 2°TA was blocked by pretreatment, but not posttreatment, with a topical μ-opioid agonist, loperamide (1.7%–5%). Second, 2°TA was blocked by intrathecal morphine (0.1–10 μg) pre- and postinjury. 2°TA reappeared when systemic naloxone was given before, but not after, injury in intrathecal morphine-pretreated rats. Intrathecal remifentanil, a short-lasting μ-opioid agonist, infused periinjury (3 μg/min), did not block subsequent primary thermal hyperalgesia, but it produced a dose-dependent (0.3–3 μg/min) abolition of 2°TA. Local tissue injury leads to 2°TA by the activation of opiate-sensitive afferents and the initiation of a cascade that persists in the absence of that initiating injury-induced stimulus.

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