The jaw-opening reflex (JOR) can be evoked by electrical stimulation of either the low- or high-threshold afferents of the trigeminal nerve. The JOR evoked by high-threshold afferents is thought to be evoked by noxious stimulation (Lund et al., 1984). We have reported that stimulation of the red nucleus (RN) facilitated the low-threshold afferent-evoked JOR and suppressed the high-threshold afferent-evoked JOR. The effect is probably mediated by an indirect pathway, since there is little evidence for direct projections from the RN to the trigeminal motor nucleus. A possible interneuronal link in this pathway could be located within the lateral reticular nucleus (LRN). This region has been proposed as a site engaged in the mechanisms of analgesia (Hall et al., 1982; Morton et al., 1983) and to receive contralateral projections from the RN (Flumerfelt and Gwyn, 1974). Furthermore, stimulation of the LRN suppressed the JOR evoked by noxious stimulation (Sotgiu, 1986). We therefore decided to examine whether lesion of the LRN affects RN-induced modulation of the JOR. The experiments were performed on 10 male Sprague-Dawley rats weighing 319-364 g. The rats were anesthetized with urethane and α-chloralose (500 m/kg and 50 mg/kg, respectively; i.p.), so as to maintain anesthesia at a level at which no withdrawal reflex was evoked by noxious stimulation of the paw. Arterial blood pressure was monitored to confirm the condition of the rat throughout the experiment. The test stimulation was applied to the inferior alveolar nerve (1 pulse, 0.1 ms in duration, 1 Hz) to evoke the JOR. The stimulus intensity was either 1.2 (low threshold) or 4.0 (high threshold) times the threshold. The electromyograms were recorded from the anterior belly of the digastric muscles. The conditioning stimulation (1pulse, 0.2 ms in duration, 1 Hz, 100 μA) was applied to the RN 10 or 30 ms before the test stimulation. The control JOR responses were recorded as well as the modulation induced by stimulation of the RN. The LRN lesion was made contralateral to the RN by the passage of electric current (20 μA, 2 min). The effect of the RN stimulation on the JOR was tested at the termination of lesion. At the end of each experiment, the stimulating sites were verified histologically. RN-induced facilitation of the JOR was not affected by lesion of the LRN (n=7, Wilcoxon t-test with Bonferroni correction, P > 0.05). On the other hand, RN-induced suppression of the JOR is significantly reduced by lesion of the LRN (n=7, Wilcoxon t-test with Bonferroni correction, P < 0.05). RN-induced modulation of the JOR was not affected by lesion of the outside of the LRN (n=3, Wilcoxon t-test with Bonferroni correction, P > 0.05).These results suggest that the suppressive effect of RN stimulation on the JOR is mediated partly by a relay in the contralateral LRN.