The paramedian pontine and bulbar tegmentum was explored by microstimulation to outline the sites of origin of direct excitatory and inhibitory inputs to lateral rectus (LR) and medial rectus (MR) motoneurons (MNs). In order to avoid activation of fibers of passage and axon reflexes originating outside the stimulation sites, experiments were carried out 4--22 days after brain stem transections causing degeneration of vestibulo-ocular pathways. Additionally, in some experiments the paramedian tegmentum was isolated from the contralateral side by midline transections. Mapping of stimulus sites from which monosynaptic EPSPs and IPSPs were elicited brought out the following preoculomotor reticular regions: 1. LR-MNs received monosynaptic IPSPs from the contralateral reticular formation corresponding to Nucl. reticularis points caudalis (R.p.c.) and the rostral part of Nucl. reticularis gigantocellularis (R.gc.). 2. Monosynaptic inhibitory input to MR-MNs could only be demonstrated after degeneration of excitatory pathways ascending from the internuclear neurons of the VIth nucleus and from the ipsilateral vestibular nuclei. Monosynaptic IPSPs originated in the ipsilateral dorso-medial tegmentum through the entire extent of the Nucl. reticularis pontis oralis and rostral R.p.c. including the region of the ipsilateral VIth nucleus. 3. Monosynaptic excitation of LR-MNs was induced by stimulation of the ipsilateral R.p.c. and the rostral half of the paramedian bulbar tegmentum (R.gc.). 4. The sites from which monosynaptic EPSPs were evoked in MR-MNs were confined to the contralateral VIth nucleus and its immediate vicinity. No evidence could be obtained for direct excitatory inputs to MR-MNs from the ipsilateral paramedian tegmentum. It is concluded that the paramedian rhombencephalic reticular formation contains four pools of premotor neurons related to coordination of conjugate horizontal eye movements. Two of them are excitatory for LR- and MR-MNs with ipsilateral ON-directions, the other two mediate reciprocal inhibition of the antagonistic motor nuclei.