Abstract
Participation of the sensory neurons, especially substance P (SP)-containing neurons, in the inflammatory response induced by formalin (FOR), croton oil (CRO), mustard oil (MUS), carrageenin (CAR), dextran (DEX) and egg white (EGG) was studied in mice and rats. FOR-induced foot edema was significantly inhibited by denervation of the sciatic nerve of rats, but it was slightly facilitated by that of the saphenous nerve. CAR-induced edema was not influenced by denervation of both nerves. In mice pretreated with capsaicin of the sciatic nerve, the early phase of foot edema induced by FOR, CRO or MUS was significantly inhibited. Edema induced by CAR, DEX or EGG was not inhibited by the capsaicin treatment. Spantide (an SP antagonist) at 0.1 mg/kg showed the same result as the capsaicin treatment. FOR, CRO or MUS caused a marked plasma extravasation, which was inhibited by spantide. The weak plasma extravasation elicited by CAR, DEX or EGG was not inhibited by spantide. FOR, CRO or MUS caused an intense biphasic nociceptive response; and the early phase of the response was inhibited by spantide. CAR, DEX or EGG caused little or no nociception. These findings suggest that SP antidromically released from the primary sensory neurons may induce potent vascular responses such as vasodilatation and plasma extravasation in the early phase of inflammation induced by FOR, CRO and MUS, whereas inflammatory responses induced by CAR, DEX and EGG may progress through different processes.
