Amputation of the mouse tail tip (2.5 cm) caused long term thermal and
mechanical hyperalgesia in the remaining part of the tail. Hyperalges
ia of the hindpaw to noxious heat (55 degrees C) and cold (0 degrees C
) stimuli were also observed. Hyperalgesia at both the tail and hindpa
w had a rapid onset (less than or equal to 30 min) and long lasting (g
reater than or equal to 7 days) effect. Skin temperature of the remain
ing 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 (less than or equal to 48 h). Intrathecal pretreatment w
ith NMDA receptor antagonists significantly attenuated long term hyper
algesia 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 i
nvestigating mechanisms of persistent pain after amputation. (C) 1998
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