Sections prepared by the Nauta and Nissl methods have been used to study the subcortical distribution of axon and cell degeneration in rabbits after lesions in visual areas I and II (V I and V II) of the cerebral cortex. Degeneration was limited to the side of the lesions. Following lesions of either V I or V II, two distinct groups of degenerating axons were traced caudally. (i) One of these groups projected through the optic tract and its subjacent nuclei. The terminal portions of its axons were found to form zones of pericellular fiber (or boutonal) degeneration in the thalamic reticular nucleus (TRN), the ventral and dorsal lateral geniculate nuclei (LGv, LGd), the pulvinar (Pul), the nuclei praetectalis anterior and posterior (dorsal and lateral parts respectively), the nucleus tractus opticus, and the superior colliculus (SC). In the TRN, LGd, Pul, and nuclei praetectalis anterior and posterior the zones of degeneration were disposed into distinct columns. After lesions involving V II the terminal portions of these axons were also seen to form zones of pericellular fiber degeneration in the nuclei praetectalis and posterior (ventral and medial parts respectively), the ventrolateral thalamic nucleus, and the zona incerta. (ii) The second group of degenerating axons traversed the cerebral peduncle and the terminal portions of its axons were shown to form zones of pericellular fiber degeneration in the basal pons. Retinotopically organized projections from V I were recognized in the LGv, LGd, Pul, nuclei praetectalis anterior and posterior (dorsal and lateral parts respectively), and SC; and the evidence reveals the presence of similarly organized projections from V II. Other retinotopically organized projections from the visual areas could not be demonstrated. The data support the view that the collateral branches of visual cortical axons serve as a principal source of input to some of the cellular components receiving innervation from the visual areas. Cellular degeneration was confined to the LGd and then present only with lesions involving V I. With each such lesion, the cellular degeneration formed a distinct column within the LGd, and this column and the one consisting of pericellular fiber (or boutonal) degeneration were consistently found to overlap.
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Giolli et al. (1971) studied this question.
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