Neurite outgrowth from bipolar and horizontal cells after experimental retinal detachment.

To study the responses of horizontal cells and rod bipolar cells, the second-order neurons in the retina, to the degeneration induced by experimental retinal detachment. Retinas from the eyes of domestic cats were examined 1, 3, 7, and 28 days after detachment using immunocytochemical and electron microscopic analyses. Retinal sections were labeled with antibodies to synaptophysin, calbindin D, and protein kinase C (PKC), proteins that serve as markers for synaptic terminals, horizontal cells, and rod bipolar cells, respectively. Beginning 1 day after detachment, the outer plexiform layer becomes disorganized and synaptophysin-labeled photoreceptor terminals are detected among the cell bodies of photoreceptors in the outer nuclear layer (ONL). At the same time, horizontal and rod bipolar cell processes grow into the ONL. In some cases, these processes contact photoreceptor terminals that have withdrawn deep into the ONL. Double-labeling experiments with antibodies to glial fibrillary acidic protein (Müller cell labeling) and phosphodiesterase gamma (cone labeling) demonstrate that the calbindin D- and PKC-positive neurite outgrowths are not derived from either Müller cells or cone photoreceptors. Horizontal and rod bipolar cell processes lengthen after retinal detachment, perhaps in response to a withdrawal of their presynaptic targets, the photoreceptor synaptic terminals. This apparent attempt to maintain synaptic contact after injury demonstrates a plasticity in the adult retina that may be of importance for the recovery of vision in human patients.