Neurochemical changes in the primate lateral geniculate nucleus following lesions of striate cortex in infancy and adulthood: implications for residual vision and blindsight

Abstract

Following lesions of the primary visual cortex (V1), the lateral geniculate nucleus (LGN) undergoes substantial cell loss due to retrograde degeneration. However, visually responsive neurons remain in the degenerated sector of LGN, and these have been implicated in mediation of residual visual capacities that remain within the affected sectors of the visual field. Using immunohistochemistry, we compared the neurochemical characteristics of LGN neurons in V1-lesioned marmoset monkeys (Callithrix jacchus) with those of non-lesioned control animals. We found that GABAergic neurons form approximately 6.5% of the neuronal population in the normal LGN, where most of these cells express the calcium-binding protein parvalbumin. Following long-term V1 lesions in adult monkeys, we observed a marked increase (~ sevenfold) in the proportion of GABA-expressing neurons in the degenerated sector of the LGN, indicating that GABAergic cells are less affected by retrograde degeneration in comparison with magno- and parvocellular projection neurons. In addition, following early postnatal V1 lesions and survival into adulthood, we found widespread expression of GABA in putative projection neurons, even outside the degenerated sectors (lesion projection zones). Our findings show that changes in the ratio of GABAergic neurons in LGN need to be taken into account in the interpretation of the mechanisms of visual abilities that survive V1 lesions in primates.

Keywords: Blindsight; Gamma amino butyric acid (GABA); Lateral geniculate nucleus; Marmoset; Occipital lesions.