Amputation of a segment of the tail produced long-lasting changes in nociception and morphine-induced antinociception. Plastic changes in nociceptive transmission may occur at the spinal cord as well as supraspinal structures after tail amputation. Acute hyperalgesia is detected at the remaining part of the tail as well as hindpaw. Morphine induced facilitation of the hot-plate (HP) response at a low dose and a greater dose of morphine is required to produce complete inhibition of the HP response. Since these effects happen at five weeks after the surgery, tail amputation may serve as a mouse model for studying long-term plastic changes in central nervous system after amputation.