NMDA receptor-dependent long term hyperalgesia after tail amputation in mice.
Amputation of the mouse tail tip (2.5 cm) caused long term thermal and mechanical hyperalgesia in the remaining part of the tail. Hyperalgesia of the hindpaw to noxious heat (55 degrees C) and cold (0 degrees C) stimuli were also observed. Hyperalgesia at both the tail and hindpaw had a rapid onset (< or = 30 min) and long lasting (> or = 7 days) effect. Skin temperature of the remaining tail or hindpaw was not significantly affected by the amputation. Heat injury of the tail in normal mice induced short but not long term hyperalgesia (< or = 48 h). Intrathecal pretreatment with NMDA receptor antagonists significantly attenuated long term hyperalgesia caused by tail amputation. These results strongly suggest that spinal NMDA receptors are critical for the induction of hyperalgesia by tail amputation, and the current mouse model may prove useful for investigating mechanisms of persistent pain after amputation.
Zhuo
M
M
Department of Anesthesiology, Washington University Medical Center, Washington University in St. Louis, MO 63110, USA. zhuom@morpheus.wustl.edu
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology / Q000627:therapeutic use; D000671:Amputation, Surgical / Q000009:adverse effects*; D000818:Animals; D016291:Dizocilpine Maleate / Q000494:pharmacology / Q000627:therapeutic use; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D006930:Hyperalgesia / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D007278:Injections, Spinal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D013623:Tail
D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D016291:Dizocilpine Maleate; D015763:2-Amino-5-phosphonovalerate