The nucleus pretectalis principalis: A pretectal structure hidden in the mammalian thalamus.

A defining feature of the amniote tecto-fugal visual pathway is a massive bilateral projection to the thalamus originating from a distinct neuronal population, tectal ganglion cells (TGCs), of the optic tectum/superior colliculus (TeO/SC). In sauropsids, the thalamic target of the tecto-fugal pathway is the nucleus rotundus thalami (Rt). TGCs axons collateralize en route to Rt to target the nucleus pretectalis principalis (PT), which in turn gives rise to bilateral projection to the TeO. In rodents, the thalamic target of these TGCs afferents is the caudal division of the pulvinar complex (PulC). No pretectal structures in receipt of TGC collaterals have been described in this group. However, Baldwin et al. (Journal of Comparative Neurology, 2011;519(6):1071-1094) reported in the squirrel a feedback projection from the PulC to the SC. Pulvino-tectal (Pul-T) cells lie at the caudal pole of the PulC, intermingled with the axonal terminals of TGCs. Here, by performing a combination of neuronal tracing, immunohistochemistry, immunofluorescence, and in situ hybridization, we characterized the pattern of projections, neurochemical profile, and genoarchitecture of Pul-T cells in the diurnal Chilean rodent Octodon degus. We found that Pul-T neurons exhibit pretectal, but not thalamic, genoarchitectonical markers, as well as hodological and neurochemical properties that match specifically those of the avian nucleus PT. Thus, we propose that Pul-T cells constitute a pretectal cell population hidden within the dorsal thalamus of mammals. Our results solve the oddity entailed by the apparent existence of a noncanonic descending sensory thalamic projection and further stress the conservative character of the tectofugal pathway.

Pax3 overexpression induces cell aggregation and perturbs commissural axon projection during embryonic spinal cord development.

Pax3 is a transcription factor that belongs to the paired box family. In the developing spinal cord it is expressed in the dorsal commissural neurons, which project ascending axons contralaterally to form proper spinal cord-brain circuitry. While it has been shown that Pax3 induces cell aggregation in vitro, little is known about the role of Pax3 in cell aggregation and spinal circuit formation in vivo. We have reported that Pax3 is involved in neuron differentiation and that its overexpression induces ectopic cadherin-7 expression. In this study we report that Pax3 overexpression also induces cell aggregation in vivo. Tissue sections and open book preparations revealed that Pax3 overexpression prevents commissural axons from projecting to the contralateral side of the spinal cord. Cells overexpressing Pax3 aggregated in cell clusters that contained shortened neurites with perturbed axon growth and elongation. Pax3-specific shRNA partially rescued the morphological change induced by Pax3 overexpression in vivo. Our results indicate that the normal expression of Pax3 is necessary for proper axonal pathway finding and commissural axon projection. In conclusion, Pax3 regulates neural circuit formation during embryonic development. J. Comp. Neurol. 525:1618-1632, 2017. © 2016 Wiley Periodicals, Inc.

Pax3 and Pax7 interact reciprocally and regulate the expression of cadherin-7 through inducing neuron differentiation in the developing chicken spinal cord.

Pax3 and Pax7 are closely related transcription factors that are widely expressed in the developing nervous system and somites. In the CNS, both genes are expressed in the dorsal part of the neural tube during development. Pax3 and Pax7 are involved in the sonic hedgehog (Shh) signaling pathway and are inhibited by Shh overexpression. The present study confirms in vivo that Pax3 overexpression represses the expression of Pax7, whereas Pax7 overexpression endogenously enhances and ectopically induces the expression of Pax3 in the developing chicken spinal cord. Overexpression of Pax3 and Pax7 represses the endogenous expression of cadherin-7, a member of the cadherin family of morphogenetic genes, and induces its ectopic expression. The present study also shows that overexpression of Pax3 and Pax7 changes the fate and morphology of cells in the neuroepithelial layer and induces the expression of postmitotic neuronal markers. We show that both Pax3 and Pax7 promote the differentiation of neural progenitor cells into neurons. Furthermore, the downregulation of Pax3 and Pax7 with specific shRNAs results in apoptosis in the developing spinal cord. Collectively, these results suggest that the transcription factors Pax3 and Pax7 play important roles in regulating morphogenesis and cell differentiation in the developing spinal cord.