Studies of visual callosal connections proposed that bilateral projections from temporal retina promote the formation of callosal linkages between cortical loci that are retinotopically matched and non-mirror symmetric with respect to the brain midline. It is therefore possible for a spontaneously active retinal locus to simultaneously activate retinotopically corresponding loci in both cortices, leading to Hebbian-like stabilization of connections between them before the eyes open. Interhemispheric correlated activity could stem from single ganglion cells that send axon branches to both sides, or from closely located cells that project to one side or the other, but which fire in synchrony due to spontaneously generated retinal activity waves. We hypothesized that lack of retinal waves could induce callosal map anomalies similar to those produced by neonatal enucleation. We studied mice lacking retinal waves due to deficiency in the ß2 subunit of the nicotinic acetylcholine receptor. The organization of callosal projections revealed with small tracer injections was correlated with V1 maps made by imaging intrinsic optical responses to drifting stimuli. Consistent with studies showing that retinofugal and geniculocortical projections are less focused in ß2 -/- mice, we found that the overall callosal pattern in V1 is markedly broader in ß2 -/- mice than in wild type mice. However, the fine topography of the callosal map in ß2 -/- mice is similar to that in wild type and ß2 -/+ mice, indicating that lack of retinal waves is not sufficient for inducing the reversal in the callosal map caused by neonatal enucleation.