The amygdala, most known for opioid-mediated pain inhibition, has recently been linked to descending pain facilitation. Specifically, the latero-capsular part of the central nucleus of the amygdala (CeA), the ‘nociceptive amygdala', exhibits enhanced excitability and synaptic plasticity in an inflammatory model of persistent pain. To test the hypothesis that the CeA contributes to behavioral signs of neuropathic pain, we transected the tibial and common peroneal branches of the left sciatic nerve, thus sparing the sural branch (spared nerve injury model), and implanted bilateral guide cannulae above the CeA in male Sprague-Dawley rats. 14 d following nerve injury, 4% lidocaine, 2% bupivacaine or saline was bilaterally injected in the CeA, followed by tests for mechanical allodynia [using von Frey hairs and a machine mounted probe (Ugo Basile)], mechanical hyperalgesia (gentle plantar application of a diaper pin), and cold allodynia (plantar application of acetone). Compared to saline, lidocaine and bupivacaine robustly reduced allodynia and hyperalgesia at the paw ipsilateral to injury (p's < .05), and did not affect responses at the contralateral paw (p's > .05). Unilateral lidocaine administration to the right CeA produced similar results, while administration to the left CeA had no effect. Experiments are in progress to determine the effects of unilateral CeA inactivation following nerve injury of the right sciatic nerve. The present results support the hypothesis that the CeA or fibers of passage play a facilitatory role in the maintenance of chronic neuropathic pain.