Calretinin in the mouse superior colliculus originates from retinal ganglion cells

We investigated the origin of the calretinin-immunoreactive fibers in the mouse superior colliculus. The dense plexus of calretinin-positive fibers in the superficial layers of the colliculus was completely eliminated after eye enucleation. Retrograde tracing combined with immunohistochemistry revealed many calretinin-positive small-to-medium retinal ganglion cells projecting to the colliculus. These results indicate that calretinin-containing ganglion cells are the source of this calcium-binding protein in the superficial layers of the superior colliculus.

Lectin histochemistry of microglia in superior colliculus of the developing opossum

The development of microglia in the opossum superior colliculus (SC) has been studied by lectin histochemistry (Griffonia simplicifolia B4 isolectin, GsI/B4). Prior to the end of neurogenesis (by postconceptional day 26, PcD 26), there are virtually no GsI/B4+ cells in the SC parenchyma although rare roundish elements are found at the tectal and, in larger numbers, the tegmental border of the aqueduct. The appearance of microglia in the SC follows a ventrodorsal gradient, correlating with the direction of neurogenesis, cytomorphological differentiation and growth of the vascular network rather than with a leptomeningeal source, and without forecasting value for astroglial differentiation. In the superficial layers (sSC), relatively few but moderately ramified cells rather than macrophages coexist with regressive changes in retinocollicular axons (by PcD 39-53). By the end of and soon after this period, there is a striking increase in the number of fairly ramiried GsI/B4+ cells within the SC proper. Macrophages also become abundant but remain restricted to the vicinity of the aqueductal ependyma and are fewer at the tectal than at the tegmental aspect. These supraependymal macrophages as well as ramified parenchymal cells maintain the ability to divide at a low rate throughout maturation. The ingress via the aqueduct and cell proliferation may contribute to the complement of SC microglia but the major immediate source remains unknown.