The recent failure of substance P receptor (NK1) antagonists in clinical trials for treatment of pain spawned additional studies asking why preclinical models implicating SP in chronic pain did not translate into a viable target for analgesic development. This review focuses on recent pain model system studies, suggesting that it is not SP or NK1 per se, but rather the cells that express NK1 that are crucial for maintaining chronic pain. © 2004 Elsevier Ltd. All rights reserved.
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