While the summit of the Antarctic Plateau has long been expected to harbor the best ground-based sites for terahertz (THz) frequency astronomical investigations, it is only recently that direct observations of exceptional THz atmospheric transmission and stability have been obtained. These observations, in combination with recent technological advancements in astronomical instrumentation and autonomous field platforms, make the recognition and realization of terahertz observatories on the high plateau feasible and timely. Here, we will explore the context of terahertz astronomy in the era of Herschel, and the crucial role that observatories on the Antarctic Plateau can play. We explore the important scientific questions to which observations from this unique environment may be most productively applied. We examine the importance and complementarity of Antarctic THz astronomy in the light of contemporary facilities such as ALMA, CCAT, SOFIA and (U)LDB ballooning. Finally, building from the roots of THz facilities in Antarctica to present efforts, we broadly highlight future facilities that will exploit the unique advantages of the Polar Plateau and provide a meaningful, lasting astrophysical legacy.

We performed genome-wide chemical mutagenesis of C57BL/6J mice using N-ethyl-N-nitrosourea (ENU). Electroretinographic screening of the third generation offspring revealed two G3 individuals from one G1 family with a normal a-wave but lacking the b-wave that we named nob4. The mutation was transmitted with a recessive mode of inheritance and mapped to chromosome 11 in a region containing the Grm6 gene, which encodes a metabotropic glutamate receptor protein, mGluR6. Sequencing confirmed a single nucleotide substitution from T to C in the Grm6 gene. The mutation is predicted to result in substitution of Pro for Ser at position 185 within the extracellular, ligand-binding domain and oocytes expressing the homologous mutation in mGluR6 did not display robust glutamate-induced currents. Retinal mRNA levels for Grm6 were not significantly reduced, but no immunoreactivity for mGluR6 protein was found. Histological and fundus evaluations of nob4 showed normal retinal morphology. In contrast, the mutation has severe consequences for visual function. In nob4 mice, fewer retinal ganglion cells (RGCs) responded to the onset (ON) of a bright full field stimulus. When ON responses could be evoked, their onset was significantly delayed. Visual acuity and contrast sensitivity, measured with optomotor responses, were reduced under both photopic and scotopic conditions. This mutant will be useful because its phenotype is similar to that of human patients with congenital stationary night blindness and will provide a tool for understanding retinal circuitry and the role of ganglion cell encoding of visual information.