Single-cell recording, electrolytic lesion and electrical stimulation studies have indicated that the pontomedullary reticular formation (PMRF) plays a role in head movement (HM) control. However, recent studies utilizing excitotoxin lesions of the PMRF have reported no effect on HM. In the present study, we have examined the acute and chronic motor effects of injecting ibotenic acid (IBO) into the nucleus reticularis pontis oralis, nucleus reticularis pontis caudalis and rostral medullary nucleus gigantocellularis of the feline PMRF. IBO injections in all of these regions induced tonic flexion of the head toward the ipsilateral side. This effect lasted 4-16 h. It was followed by a second phase in which head flexion and whole body circling were directed toward the contralateral side. Although this forced contralateral head turning disappeared within two days, the tendency to turn contralaterally and the impaired ability to make rapid ipsilateral HMs were present throughout survival periods lasting more than 4 months. Unilateral IBO PMRF lesions reduced the amplitude of vestibular induced quick phase (anti-compensatory) HMs toward the ipsilateral side and resulted in abnormally large and persistent slow compensatory HMs toward the contralateral side. Following IBO injections, the threshold intensity for HMs evoked by electrical stimulation at the injection site was elevated, and the amplitude and velocity of evoked HMs reduced. Histological data indicated that the reticular area involved in HM control was relatively large and probably extended beyond the PMRF region examined here. However, lesions including the nucleus reticularis pontis caudalis (NRPC) produced more severe and persistent HM deficits than those including the nucleus reticularis gigantocellularis. These data together with available anatomical and electrophysiological evidence indicate that PMRF neurons play a critical role in the generation of fast horizontal HMs toward the ipsilateral side.