The present study was designed to investigate a possible role of
vanilloid receptors, CGRP and spleen in the induction of diabetes induced
hyperalgesia in mice. Tail flick latency, an index of
hyperalgesia, was assessed using analgesiometer. Serum
nitrite levels and an index of
nitric oxide were analyzed using Griess reaction. Mice were rendered diabetic with
streptozotocin (200 mg/kg(-1), i.p.) and kept for 30 days for development of diabetic
pain. To explore the involvement of spleen in diabetic
pain, spleen homogenate supernatant (SHS) was prepared from spleen of 30th day diabetic mice and administered in normal mice for 14 days. Both in diabetic and SHS treated mice, significant degree of
hyperalgesia was developed, suggesting the possible role of spleen derived factor in induction of diabetic
pain. Moreover, the levels of
nitric oxide were also elevated in 30 day diabetic mice and SHS treated mice. Administration of
ruthenium red (1 mg/kg(-1), i.p.),
vanilloid receptor antagonist, and
sumatriptan (50 mg/kg(-1), i.p.), a CGRP release inhibitor, attenuated diabetes and SHS induced decrease in nociceptive threshold and increase in serum
nitrite oxide levels. These results suggest that spleen derived factor induced activation of
vanilloid receptors and CGRP release may be contributing in the development of
hyperalgesia in diabetic mice.