Abstract
Hemokinin-1 mainly acts on the neurokinin-1 (NK1) receptors and is involved in the pain transmission like substance P. Transient receptor potential vanilloid 1 (TRPV1) channel are activated by various factors, but it has not been reported that TRPV1 channel is activated by hemokinin-1. We found that the nociceptive behaviors by intrathecally (i.t.) administered hemokinin-1 in mice were caused through TRPV1 channel.
The nociceptive behaviors induced by i.t. administered hemokinin-1 were observed directed biting and licking along with both hindlimb scratching in mice and recorded as the total response times of these nociceptive behaviors. In order to confirm that Hemokinin-1 activated TRPV1, the amount of phosphorylated TRPV1 was measured by Western blot analysis.
The nociceptive behaviors induced by i.t. administered hemokinin-1 was decreased by capsazepine, a TRPV1 channel antagonist. Pretreatment with antiserum against TRPV1 channel was eliminated the nociceptive behaviors induced by i.t. administered hemokinin-1. The phosphorylation of TRPV1 channel in the spinal dorsal horn was increased by i.t. administered hemokinin-1. These results show that hemokinin-1, unlike substance P, elicits the nociceptive behaviors by TRPV1 channel as well as NK1 receptor on spinal dorsal horn.
