In order to analyze the role of lamination in establishing the precisely ordered connectional pattern of the neocortex, we compared the afferent and efferent connections of the visual cortical areas in normal mice with those of the mutant mouse reeler (rl). The reeler mutation causes disruption of the laminar organization of the neocortex; all classes of neurons are present but are abnormally located. The corticocortical and thalamocortical connection os visual cortical areas 17, 18a, and 18b were determined in normal and reeler mice with injections of horseradish peroxidase (HRP) or HRP conjugated with wheat germ agglutinin (HRP-WGA). The diffusion of HRP-WGA is highly restricted due to the surface binding properties of the lectin; it was particularly effective in demonstrating retinotopically ordered connections. We found that the patterns of connections made the reeler mutant are indistinguishable from normal. Cortical loci in area 17 are reciprocally connected to homotopic locations in areas 18a and 18b. Area 17 is also reciprocally connected with dorsal lateral geniculate nucleus of the thalamus and projects to the superior colliculus. Areas 18a and 18b are reciprocally connected with each other and with the lateral posterior and lateral nuclei of the thalamus, respectively. In addition, we found evidence of reciprocal connections between the lateral posterior nucleus and area 17, and between the lateral nucleus and areas 17 and 18a. The results indicate the neurons in visual cortical areas of the reeler mutant mouse are capable of forming retinotopically organized corticocortical and thalamocortical connections in a pattern similar to that found in normal animals. Thus the genetic anomaly producing incorrect neuronal positioning during development of the reeler cortex does not seriously impede the pathway and target recognition mechanisms responsible for formation of functionally appropriate cortical connections.