Neuroprogenitor cells in the developing retina extend processes, which stretch from the basal vitread surface to the apical ventricular surface. During the cell cycle, the nucleus undergoes interkinetic migration, moving in a vitread direction during G1, passing through S-phase at its peak and then, on entering G2, returning towards the ventricular surface where it will enter M-phase and divide. We have previously shown that individual saltatory movements of the nucleus correlate with calcium events within the progenitor cells and that these events spread to neighbouring progenitor cells through connexin43 (Cx43) gap junction channels, thereby coordinating the migration of coupled clusters of cells. Disrupting coupling by pharmacological agents or molecular means with Cx43-specific antisense oligodeoxynucleotides (asODNs) or dominant negative Cx43 (dnCx43) inhibits the sharing of calcium events, reducing the number that each cell experiences, and significantly slows their interkinetic migration. Monitoring the location within the retina of progenitor cells that were transfected with GFP-dnCx43 24 hours previously, we find 70% of them to be located, at the ventricular surface of the retina, where mitosis normally takes place. A similar effect was produced in eGFP-transfected progenitor cells in retinae that had been treated with Cx43-specific asODNs or cultured in the presence of pharmacological blockers of gap junctional communication. These findings potentially imply either that more progenitor cells were undergoing mitosis in conditions of reduced communication or that they were taking longer to go about it. Closer examination of the GFP-transfected cells at the ventricular surface revealed that they had begun to grow neurites, implying that they had differentiated ectopically, having failed to migrate away from the ventricular surface towards the vitread surface of the retina as differentiating neurons should. Immunostaining of untransfected retinae with the neuronal marker TuJ1 after overnight treatment with Cx43asODNs or pharmacological gap junctional blockers revealed strong staining at the ventricular surface which was not seen in control retinae. These findings imply that blocking communication prevents cells from migrating away from the ventricular zone, either by interfering with the migration mechanism prior to neuritogenesis or by causing the precocious differentiation of neurites which prevent subsequent migration. Clearly, appropriate levels of gap junctional communication between retinal neuroprogenitor cells are essential for their normal cell cycle progression, differentiiaton and migration to appropriate terminal sites. Other parts of the CNS, such as the cerebral cortex, undergo similar processes during development, so it is likely that gap junctional communication has a fundamental role in the proliferation, differentiation and migration of neurons throughout the CNS, coordinating the formation of its normal architecture.