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The morphology of retinogeniculate X- and Y-cell axonal arbors in dark-reared cats
Insights
Visual deprivation in cats, like dark-rearing, reduces Y-cells in the lateral geniculate nucleus. However, retinogeniculate axon morphology appears normal, suggesting other factors cause this Y-cell loss.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Visual System Development
Background:
- The cat's retinogeniculate pathway matures postnatally.
- Visual deprivation impacts this maturation, causing abnormalities.
- Monocular suture and dark-rearing reduce Y-cells in the lateral geniculate nucleus.
Purpose of the Study:
- To investigate the morphology of retinogeniculate axons in dark-reared cats.
- To determine if axon morphology differences explain the reduction in Y-cells.
Main Methods:
- Dark-reared cats were used.
- Horseradish peroxidase was injected into identified retinogeniculate axons.
- Extracellular recording was used to identify geniculate Y-cells.
Main Results:
- Retinogeniculate X- and Y-cell axons in dark-reared cats showed normal morphology.
- The proportion of physiologically identified geniculate Y-cells was reduced in dark-reared cats compared to normal cats.
- This finding contrasts with observations in monocularly sutured cats.
Conclusions:
- Normal retinogeniculate axon morphology in dark-reared cats suggests the Y-cell reduction is not due to axonal abnormalities.
- Potential causes for Y-cell loss include conduction block, inhibition, or altered non-retinal influences.
- Visual deprivation affects Y-cell development through mechanisms beyond retinogeniculate axon morphology.
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 dark-reared cats. Surprisingly, we found that our sample of retinogeniculate X- and Y-cell axons in dark-reared 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.