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Lesions in the primary visual cortex (V1) cause extensive retrograde degeneration in the lateral geniculate nucleus, but it remains unclear whether they also trigger any neuronal loss in other subcortical visual centers. The inferior (IPul) and lateral (LPul) pulvinar nuclei have been regarded as part of the pathways that convey visual information to both V1 and extrastriate cortex. Here, we apply stereological analysis techniques to NeuN-stained sections of marmoset brain, in order to investigate whether the volume of these nuclei, and the number of neurons they comprise, change following unilateral long-term V1 lesions. For comparison, the medial pulvinar nucleus (MPul), which has no connections with V1, was also studied. Compared to control animals, animals with lesions incurred either 6 weeks after birth or in adulthood showed significant LPul volume loss following long (> 11 months) survival times. However, no obvious areas of neuronal degeneration were observed. In addition, estimates of neuronal density in lesioned hemispheres were similar to those in the non-lesioned hemispheres of same animals. Our results support the view that, in marked contrast with the geniculocortical projection, the pulvinar pathway is largely spared from the most severe long-term effects of V1 lesions, whether incurred in early postnatal or adult life. This difference can be linked to the more divergent pattern of pulvinar connectivity to the visual cortex, including strong reciprocal connections with extrastriate areas. The results also caution against interpretation of volume loss in brain structures as a marker for neuronal degeneration., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The Kv3.1b potassium channel subunit, which facilitates the fast-spiking phenotype characteristic of parvalbumin (PV)-expressing inhibitory interneurons, is also expressed by subpopulations of excitatory neurons in macaque cortex. We have previously shown that V1 neurons expressing Kv3.1b but not PV or GABA were largely concentrated within layers 4Cα and 4B of V1, suggesting laminar or pathway specificity. In the current study, the distribution and pattern of co-immunoreactivity of GABA, PV, and Kv3.1b across layers in extrastriate cortical areas V2 and MT of the macaque monkey were measured using the same triple immunofluorescence labeling, confocal microscopy, and partially automated cell-counting strategies used in V1. For comparison, densities of the overall cell and neuronal populations were also measured for each layer of V2 and MT using tissue sections immunofluorescence labeled for the pan-neuronal marker NeuN. GABAergic neurons accounted for 14% of the total neuronal population in V2 and 25% in MT. Neurons expressing Kv3.1b but neither GABA nor PV were present in both areas. This subpopulation was most prevalent in the lowest subcompartment of layer 3, comprising 5% of the total neuronal population in layer 3C of both areas, and 41% and 36% of all Kv3.1b+ neurons in this layer in V2 and MT, respectively. The prevalence and laminar distribution of this subpopulation were remarkably consistent between V2 and MT and showed a striking similarity to the patterns observed previously in V1, suggesting a common contribution to the cortical circuit across areas.