Peripheral
inflammation leads to ipsilateral and contralateral
mechanical hyperalgesia. The
transient receptor potential channel vanilloid type 1 (TRPV1), a nonselective
cation channel expressed in mammalian primary sensory neurons and the spinal cord, may be involved in peripheral
inflammation, but there is no consensus on the role of this channel in
inflammation-induced
mechanical hyperalgesia. Here, we examined the role of TRPV1 channels in
carrageenan-induced
mechanical hyperalgesia using wild-type and TRPV1-knockout (KO) mice and compared the results with those obtained in mice peripherally administered
capsazepine, a TRPV1 antagonist, or
capsaicin, a TRPV1 agonist. In the TRPV1-KO mice, ipsilateral
mechanical hyperalgesia was significantly reduced during the acute phase (10-60 min), and the contralateral
mechanical hyperalgesia nearly disappeared during both the acute and subacute phases. Blocking peripheral TRPV1 using
capsazepine before
carrageenan administration resulted in similar effects as those observed in the TRPV1-KO mice, except that it was less effective against contralateral
mechanical hyperalgesia during the subacute phase. In contrast,
capsaicin remarkably decreased ipsilateral and contralateral
mechanical hyperalgesia throughout both phases, but this
analgesic effect was not observed in the TRPV1-KO mice. Thus, TRPV1 channels could be involved in the development of both ipsilateral and contralateral
mechanical hyperalgesia after
inflammation. Peripheral TRPV1 could participate in acute
hyperalgesia, whereas central TRPV1 may participate in subacute secondary
hyperalgesia.
Capsaicin potentially acts on both primary and secondary
hyperalgesia in a TRPV1-dependent manner.