Fig 4.

Rats received dural administration of IM or SIF and α-CGRP_(8–37) (0.45 mg/kg, i.v.) 30 min afterwards (A). Systemic administration of α-CGRP_(8–37) abolished behavioral signs of tactile allodynia of the face and hindpaws, indicated by significant (P < 0.05, shown as *) reductions in normalized allodynic responses. In a second set of studies, the NK-1 antagonist L-732,138 (10 mg/kg, s.c.) was administered 10 min before dural administration of IM (B). Pretreatment with L-732,138 failed to prevent development of behavioral signs of tactile allodynia of the face or hindpaws (B). In order to test that the dose employed was sufficient to block NK-1 agonist activity, male rats received an intraplantar injection of 100 µl containing 10 µg of capsaicin and challenged with either vehicle (70% DMSO in saline) or L-732,138. Time spent licking or guarding the hindpaw was determined over a 10 min period. Capsaicin treatment after vehicle injection produced a mean cumulative response time of 133 ± 33.3 sec. Rats injected with L-732,138 showed a significantly (P < 0.05) reduced mean cumulative response time of 46 ± 14.7 sec, suggesting that the dose of L-732,138 was sufficient to block NK-1 mediated nociceptive activity (data not shown).