The albino retina is abnormal. The central region is under-developed and some cell populations are reduced or increased in number. Not least of these anomalies is the deficit in the rod population in hypopigmented rodents and carnivores. Given this abnormality we have examined the distribution of rod bipolar cells in albino rats to determine whether this subsequent stage in the rod pathway is similarly disrupted. A monoclonal antibody to protein kinase C was used to determine the distribution of rod bipolar cells in juvenile and adult pigmented and albino rats. Immunoreactive rod bipolar cells and their processes were counted in transverse sections passing through both the central and peripheral retina. The mean densities of immunoreactive cells were significantly reduced in albino retinas at both juvenile (postnatal day 15) and adult stages, in the former by 14% and the latter by 9%. This was evident across the entire central-to-peripheral extent of the retina. The reduced rod photoreceptor population found in albinos appears therefore to be consequential for the magnitude of their major target population, rod bipolar cells. The decrease in the rod bipolar population indicates a change in retinal cytoarchitecture and implies a disruption of functional organization of the albino retina, especially that underlying the scotopic channel. This, coupled with observations that some other retinal interneuronal populations may be disrupted, implies disordered retinal processing in albinos and emphasizes the likelihood that abnormal visual function in albinos may be as much a result of anomalous retinal circuitry as of the known photoreceptor deficit or chiasmatic misrouting.

Purpose:  In the retina of albino mammals so far examined there is a deficit in the rod photoreceptor population. We reasoned that a consequence of the rod deficit might be a subsequent abnormality in the next level of the rod pathway, the rod bipolar cell. We therefore compared the distribution of rod bipolar cells in pigmented and albino rats. Methods:  Rod bipolar cells were labelled in 15 µm thick sections of fixed retinas with a monoclonal antibody directed against protein kinase C, and visualized using the ABC method. Counts of the cell bodies and processes of rod bipolar cells were undertaken at various locations across the retina. Results:  Qualitatively, the protein kinase C staining suggested differences between the albino and pigmented phenotypes both in the outer and inner plexiform layers and in the inner nuclear layer. Staining was denser in the pigmented retina and the bipolar cell bodies were arranged in multiple rows rather than a single row as found in the albino retina. The actual number of rod bipolar cells was reduced in the albino phenotype. At the neonatal age we examined (post‐natal day 15), there was a 14% reduction in the total number whereas in the adult retina the reduction was around 9%. Conclusions:  Although the reduction in the rod bipolar population is not as great as that previously found for the rod photoreceptors (∼25%), the reduction in both populations suggests a general abnormality in the rod pathway of albinos. Further, our data support the view that melanin is crucially involved in the normal development of retinal structure.