A re-examination of anatomical plasticity in the rat retina

Abstract

Previous investigators have reported an increase in numbers of amacrine synapses in the inner plexiform layer (IPL) of the rat retina following light deprivation, and an increase in amacrine along with a decrease in bipolar synapses following light damage. Since there are several points of disagreement between the published reports on this subject we undertook a more detailed study of the effects of light deprivation and light damage on the retina. Four groups of eight male albino rat pups (14 days old) were raised for eight weeks under different conditions: (1) unsutured, bright light reared (UB); (2) bilaterally lid‐sutured, bright light reared (SB); (3) unsutured, low light reared (UL); and (4) bilaterally lid‐sutured, dark reared (SD). The intensity of the light given the UL group was equated with that striking the corneas of the SB group. Light microscopy showed that the retinas of the SB as well as the UB groups had almost complete degeneration of the outer retinal layers, indicating that even low intensity light, when continuous, causes severe retinal damage. The SD group was thicker in many of the retinal layers compared to the UL (control) group. Electron microscopy revealed that there were no significant changes in the incidences of any type of synapse in the IPL following light deprivation or light damage when averaged over total depth. This is in contradiction to the reports of other investigators. However, when the IPL was analyzed by levels, the incidence of amacrine‐ganglion synapses was significantly greater (p < 0.05) in groups UB and SD, but only in the outer third of the IPL. Thus, extensive postnatal plasticity of IPL synapses in the rat retina did not occur under our experimental conditions. We found, at best, only limited effects which were confined to the amacrine‐ganglion synapses.