Calbindin immunoreactivity in the geniculo-extrastriate system of the macaque: implications for heterogeneity in the...

Although most projection neurons in the primate dorsal lateral geniculate nucleus (dLGN) target striate cortex (V1), a small number project instead to extrastriate visual areas and have been suggested to play a role in the preserved vision ("blindsight") that survives damage to V1. Moreover, the distribution of dLGN cells projecting to extrastriate bears a striking similarity to that of neurons that stain for calbindin D-28K (Cal), a calcium-binding protein involved in regulating neuronal excitability and considered a marker for the koniocellular or "K" pathway of geniculocortical processing. In these studies, we used double-labeling techniques to examine whether Cal content characterizes all or a subset of neurons making up the geniculo-extrastriate pathway in normal macaque monkeys. After injections of cholera toxin B-subunit into the prelunate gyrus, the proportion of retrogradely labeled neurons in the dLGN that were also immunoreactive for Cal varied from less than 40% to over 80%, indicating that only a subset of the geniculo-extrastriate projection falls within the K pathway as defined by Cal content. Analysis of the injected territories indicated that identity of the extrastriate cortical target may be systematically related to Cal content in the geniculo-extrastriate projection. To see whether the Cal-immunoreactive dLGN population might potentially play a role in preserved vision after V1 damage, we also examined the dLGN of a macaque that had sustained a lesion of V1 in infancy and survived until 4 years. In this animal, large, intensely Cal-immunoreactive neurons were found scattered throughout the otherwise degenerated dLGN zones and made up over 95% of the identifiable remaining neurons. The results support an emerging view that the macaque koniocellular system is highly heterogeneous in nature and also suggest that Cal content may be a critical feature of the pathway by which visual information reaches extrastriate cortex in the absence of V1.