Involvement of NK-1 and NK-2 tachykinin receptor mechanisms in jaw muscle activity reflexly evoked by inflammatory irritant application to the rat temporomandibular joint

An electromyographic (EMG) study was carried out in 51 anesthetized rats to assess if neurokinin, NK-1 and NK-2, receptor mechanisms and tachykinins were involved in the increased jaw muscle activity which can be reflexly evoked by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint (TMJ) region. A baseline level of EMG activity was recorded bilaterally for 20 min from digastric (DIG) and masseter (MASS) muscles and then each animal was treated with NK-1 or NK-2 antagonist or vehicle. In one series of experiments either the NK-1 antagonist CP-99,994 (20 mu g similar to 54 nmol), the NK-2 antagonist MEN-10,376 (10 mu g similar to 9 nmol or 20 mu g similar to 18 nmol) or vehicle (control) was administrated into the lateral ventricle (i.c.v.); in another series the NK-L antagonist (4 mg/kg similar to 3-4 mu mol/rat) or vehicle (control) was given intravenously (i.v.). After 10 min, MO (20 mu l, 20%) was applied to one TMJ (first injection) and 45 min later, MO was applied to the opposite TMJ (second injection). Pretreatment with neurokinin antagonists had little effect on the incidence of the MO-evoked EMG responses but did significantly reduce the EMG magnitude and duration. In the animals pretreated with NK-1 antagonist only the responses to the second MO injection was significantly affected whereas NK-2 pretreatment reduced the EMG responses to both MO injections to the TMJ. The systematic depression of the MO-evoked EMG responses by the NK-2 antagonist suggests that neurokinin A may be involved in the EMG responses. Since the NK-1 antagonist produced no systematic changes in responses elicited by the first MO injection, substance P does not seem to be associated directly with the initiation or maintenance of the EMG responses but may be involved if a 'central sensitization' has been induced by the first MO injection to the TMJ. (C) 1998 International Association for the Study of Pain. Published by Elsevier Science B.V.