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  • Title: Morphology of single, physiologically identified retinogeniculate Y-cell axons in the cat following damage to visual cortex at birth.
    Author: Weber AJ, Kail RE, Stanford LR.
    Journal: J Comp Neurol; 1989 Apr 15; 282(3):446-55. PubMed ID: 2715392.
    Abstract:
    It has been reported previously that neurons in the dorsal lateral geniculate nucleus (LGN) of cats with neonatal damage to visual cortex (KVC cats) have receptive fields that are abnormally large and that the receptive fields of these neurons sometimes do not appear to conform to the normal retinotopic order in the LGN. A primary aim of this study was to determine if these physiological abnormalities are related to inappropriate patterns of retinogeniculate connections. We therefore have analyzed the terminal arbors of retinogeniculate axons in adult cats that had received a lesion of visual cortex (areas 17, 18, and 19) on the day of birth. Single retinogeniculate axons were characterized physiologically and injected intracellularly with horseradish peroxidase. Consistent with earlier reports that neonatal removal of visual cortex results in a retrograde loss of retinal X-cells, all of the retinogeniculate axons that we recorded were from Y-cells. While the visual responses of these Y-cell axons were normal, the morphology of their terminal arbors in the LGN was abnormal. Retinal Y-cell axons in KVC cats have terminal fields in the A laminae of the LGN that are as large or larger than those of normal Y-cells. However, since the LGN in KVC cats is severely degenerated, single Y-cell arbors occupy a proportional volume of the LGN that is 12 times greater than normal. Thus an early lesion of visual cortex produces a severe mismatch between retinogeniculate axon arbor size and target size. Also, despite the normal size of retinogeniculate axon arbors in KVC cats, the number and density of terminal boutons are greatly decreased. Thus our morphological results suggest that the unusually large receptive fields of LGN cells in KVC cats and the relative lack of retinotopic precision in the LGN are due, at least in part, to anomalies in the relative size and distribution of retinogeniculate axon arbors that develop after neonatal removal of visual cortex.
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