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PAIN MEDICINE

Differential Analgesic Sensitivity of Two Distinct Neuropathic Pain Models

Isabelle Decosterd, MD^*,, Andrew Allchorne, and Clifford J. Woolf, MD PhD

*Anesthesiology Pain Research Group, Department of Anesthesiology, University Hospital Lausanne (CHUV), Lausanne, Switzerland; Department of Cell Biology and Morphology, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland; and Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts

Address correspondence and reprint requests to Isabelle Decosterd, MD, Department of Anesthesiology & DBCM, University of Lausanne, Bugnon 9, 1005 Lausanne, Switzerland. Address e-mail to Isabelle.Decosterd{at}chuv.hospvd.ch

Progressive tactile hypersensitivity (PTH) manifesting after sciatic nerve crush and spared nerve injury (SNI) are two distinct rodent experimental models of neuropathic pain. PTH develops months after recovery from the nerve crush in response to repeated intermittent low-threshold mechanical stimulation of the reinnervated sciatic nerve skin territory and represents a model of stimulus-induced pain. SNI is characterized by an early and sustained increase in stimulus-evoked pain sensitivity in the intact skin territory of the spared sural nerve after sectioning of the two other terminal branches of the sciatic nerve. We examined the effects of morphine (0.5–10 mg/kg), gabapentin (30–200 mg/kg), MK801 (0.01–0.02 mg/kg), amitriptyline (10–25 mg/kg), and carbamazepine (5–7.5 mg/kg) in both models. Morphine, gabapentin, and carbamazepine both reversed and prevented stimulus-induced PTH, whereas MK801 and amitriptyline reduced but did not prevent stimulus-induced PTH. In contrast, the stimulus-evoked behavioral hypersensitivity in the SNI model was poorly modified by these drugs. Independent neuropathic pain models show differential sensitivity to analgesic drug treatment. We suggest that this is due to the different mechanisms responsible for the neuropathic pain-related behavior. Multiple models are required, therefore, to study the mechanisms that contribute to neuropathic pain and to predict analgesic efficacy for different components of the neuropathic pain syndrome.

IMPLICATIONS: Analgesic effects of drugs often used for the treatment of neuropathic pain were evaluated in two independent animal models of neuropathic pain. The differential analgesic response between models suggests that different mechanisms are involved and that multiple models are required to study mechanisms and predict drug efficacy for neuropathic pain.

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