It has been previously assumed that the asymmetry of the monocular optokinetic nystagmus (OKN) of lateral-eyed mammals is caused by an absence of visual cortex projections to directional selective neurons in the pretectal nucleus of the optic tract and dorsal terminal nucleus of the accessory optic system (NOT-DTN). In contrast to this generally accepted hypothesis, we present multiple evidence that OKN-related neurons in the rat NOT-DTN in fact do receive input from the visual cortex. We studied the corticofugal projection to NOT-DTN physiologically, with extracellular single unit recording and electrical stimulation of the optic chiasma and the visual cortex, and anatomically, using retrograde and anterograde tracing techniques. In particular we focussed our attention on the NOT-DTN neurons, which control eye movements during OKN. All OKN-related NOT-DTN cells were activated after optic chiasma stimulation. Forty-five percent of these neurons were also activated after stimulation of the visual cortex (VC). The majority of neurons activated from VC (80%) also responded to monocular stimulation of either eye. On the contrary, most of the neurons that responded to stimulation of the contralateral eye only were not activated from VC. After injection of fluorescent latex microspheres into the NOT-DTN, retrogradely labeled neurons were found in areas 17, 18, and 18A of the visual cortex. Phaseolus vulgaris leucoagglutinin injected into the visual cortex anterogradely labeled fibres and terminals throughout the NOT-DTN complex. Labeled boutons were found in close proximity to OKN-related NOT-DTN cells, selectively stained after horseradish peroxidase (HRP) injections into the inferior olive. Our results demonstrate that NOT-DTN cells in the rat, which are involved in the generation of horizontal OKN, receive a direct input from the ipsilateral visual cortex.