The morphology of retinogeniculate X-and Y-cell axonal arbors in dark-reared cats

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Abstract
The cat's retinogeniculate pathway, immature at birth, develops physiologically and anatomically over the first three postnatal months. Visual deprivation from birth interferes with this maturation. Thus, monocular eye lid suture from birth leads to pronounced abnormalities in the morphology of retinogeniculate terminations and geniculate neurons, and to a reduction in the proportions of Y-cells recorded physiologically in the lateral geniculate nucleus (e.g. see Sherman and Spear 1982). This “loss” of geniculate Y-cells could possibly be due to reduced retinogeniculate Y-cell terminations and expanded X-cell terminations in the A-laminae (Sur et al. 1982), so that many geniculate cells that normally receive retinal Y-cell input accept and retain retinal X-cell input (Friedlander et al. 1982). Dark-rearing from birth also leads to a reduction in the proportions of Y-cells recorded in the lateral geniculate nucleus (Kratz et al. 1979). Such a loss might also be due to abnormalities in retinogeniculate X- and Y-cell terminations. To test this possibility, we injected horseradish peroxidase into physiologically identified retinogeniculate axons of darkreared cats. Surprisingly, we found that our sample of retinogeniculate X- and Y-cell axons in darkreared cats had normal morphology. If our sample is representative of the entire population of retinogeniculate X- and Y-cell axons, retinogeniculate axon morphology in dark-reared cats differs from that in monocularly sutured cats. Yet, using extracellular recording, we replicated the observation that physiologically identified geniculate Y-cells are encountered less often in dark-reared cats than in normal cats. Given the apparent normality of the retinogeniculate axons in these cats, the “loss” of geniculate Y-cells in dark-reared cats could then conceivably be due to conduction block in retinogeniculate afferents, tonic inhibition on Y-cells, or deficits in non-retinal influences that may importantly affect Y-cell development.