Substance P receptor (SPR)-expressing spinal neurons were ablated with the
selective cytotoxin substance P-saporin. Loss of these neurons resulted in
a reduction of thermal hyperalgesia and mechanical allodynia associated wit
h persistent neuropathic and inflammatory pain states. This Loss appeared t
o be permanent. Responses to mildly painful stimuli and morphine analgesia
were unaffected by this treatment. These results identify a target for trea
ting persistent pain and suggest that the small population of SPR-expressin
g neurons in the dorsal horn of the spinal cord plays a pivotal role in the
generation and maintenance of chronic neuropathic and inflammatory pain.