Neural Plasticity in the Lateral Geniculate Nucleus Following Lesion to the Primary Visual Cortex in Macaque Monkeys Open Access

Auerbach, Aliyah (Spring 2020)

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Following lesion to primary visual cortex (V1) in macaque monkeys, retrograde degeneration occurs in neurons that project to V1 in the lateral geniculate nucleus (LGN). Lesion of V1 results in blindness to the visual field. Despite this “blindness”,  certain individuals retain residual visual capacity allowing them to implicit decisions about stimuli without awareness of their presence, a condition called blindsight. This remaining visual function is thought to be mediated by the LGN, in which interlaminar cells are implicated. We sought to determine what mediates the survival of these primarily calbindin-rich interlaminar LGN neurons following V1 lesion. Six macaque monkeys were used, four lesioned at infancy and two at adulthood. We hypothesized that surviving cells in the LGN survive because of their proximity to blood vessels. Our prediction was that the distance of a surviving cell from the nearest blood vessel in the degenerated LGN to be less than expected by chance and to be less than that of randomly selected cells in the corresponding intact LGN section. Our second hypothesis was that cells that fall within a zone of high retinal innervation are more likely to survive degeneration and we predicted that surviving cells would be preferentially located in an area of high retinal input compared with randomly selected cells in the intact LGN. Our results showed that surviving cells were not significantly closer to blood vessels than by chance or in the correlated intact LGN, and only one of the five subjects showed significant preferential clustering in areas of high retinal innervation post-lesion. Therefore, the results of our experiments did not support either hypothesis. However, we did find that adult-lesion surviving cells were significantly closer to blood vessels than infant-lesion surviving cells post-lesion and adult-lesion animals contained a significantly higher proportion of calbindin-negative surviving cells than infant-lesion animals. As such, future directions could involve looking further into distinguishing characteristics of these calbindin-negative cells that survive, the effects of age and other individual differences that may account for these results, and possible dendritic branching of surviving cells post-lesion. 

Table of Contents

Table of Contents

Introduction. 1

Blindsight and Behavior. 1

Relevant Neuroanatomy of the Visual System. 3

Hypotheses and Predictions. 6

Materials and Methods. 8

Results. 12

Discussion. 14

Distance from Blood Vessel Hypothesis. 14

Retinal Innervation Hypothesis. 17

Implications, Future Directions, and Conclusion. 19

Tables and Figures. 23

Table 1: Table of identifying information for all six subjects. 23

Figure 1: Diagram of the primary and secondary visual pathways. 24

Figure 2: Representative section of the unlesioned LGN of subject RMS-3. 25

Figure 3: Comparison of overall average distance from blood vessels in both spared cells and corresponding random points for all infant-lesion cases. 26

Figure 4: Comparison of overall average distance from blood vessels in both spared cells and corresponding random points for all adult-lesion cases. 27

Figure 5: Comparison of distance from surviving cell to blood vessel in degenerated LGN of both infant- and adult-lesion cases. 28

Figure 6: Comparison of surviving calbindin-positive cells in the degenerated LGN to randomly selected calbindin-positive cells in the intact LGN.. 29

Figure 7: Classification of surviving cells in adult-lesion animals: calbindin-positive or negative. 30

Figure 8: Classification of surviving cells in adult-lesion animals: calbindin-positive or negative. 31

Figure 9: Average difference in percentage of surviving cells in area of high retinal innervation across all sections. 32

Figure 10: Comparison of cell location distribution in the DEZ of intact LGN and corresponding surviving calbindin-positive cells in degenerated LGN for all infant-lesion subjects. 33

References. 34

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