Rapid degeneration and neurochemical plasticity of the lateral geniculate nucleus following lesions of the primary visual cortex in marmoset monkeys.

Lesions of the primary visual cortex (V1) cause retrograde neuronal degeneration, volume loss and neurochemical changes in the lateral geniculate nucleus (LGN). Here we characterised the timeline of these processes in adult marmoset monkeys, after various recovery times following unilateral V1 lesions. Observations in NeuN-stained sections obtained from animals with short recovery times (2, 3 or 14 days) showed that the volume and neuronal density in the LGN ipsilateral to the lesions were similar to those in the contralateral hemispheres. However, neuronal density in the lesion projection zone of LGN dropped rapidly thereafter, with approximately 50% of the population lost within a month post-lesion. This level of neuronal loss remained stable for over three years post-lesion. In comparison, shrinkage of the LGN volume progressed more gradually, not reaching a stable value until 6 months post lesion. We also determined the time course of the expression of the calcium-binding protein calbindin (CB) in magnocellular (M) and parvocellular (P) layer neurons, a form of neurochemical plasticity previously reported to be triggered by V1 lesions. We found that CB expression could be detected in surviving M and P neurons as early as two weeks after lesion, with the percentage of neurons showing this neurochemical phenotype gradually increasing over 6 months. Thus, neurochemical change precedes neuronal degeneration, suggesting it may be linked to a protective mechanism. This study highlights the limited time window for any possible interventions aimed at reducing secondary neuronal loss in the visual afferent pathways following damage to V1.