{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:34:52Z","timestamp":1791228892090,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"18","license":[{"start":{"date-parts":[[2008,9,15]],"date-time":"2008-09-15T00:00:00Z","timestamp":1221436800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,9,15]]},"abstract":"<jats:p>An electroretinogram (ERG) screen identified a mouse with a normal a\u2010wave but lacking a b\u2010wave, and as such it was designated <jats:italic>no b\u2010wave3<\/jats:italic> (<jats:italic>nob3<\/jats:italic>). The <jats:italic>nob3<\/jats:italic> phenotype mapped to chromosome 11 in a region containing the metabotropic glutamate receptor 6 gene (<jats:italic>Grm6<\/jats:italic>). Sequence analyses of cDNA identified a splicing error in <jats:italic>Grm6<\/jats:italic>, introducing an insertion and an early stop codon into the mRNA of affected mice (designated <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic>). Immunohistochemistry of the <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> retina showed that GRM6 was absent. The ERG and visual behaviour abnormalities of <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> mice are similar to <jats:italic>Grm6<jats:sup>nob4<\/jats:sup><\/jats:italic> animals, and similar deficits were seen in compound heterozygotes (<jats:italic>Grm6<jats:sup>nob4\/nob3<\/jats:sup><\/jats:italic>), indicating that <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> is allelic to <jats:italic>Grm6<jats:sup>nob4<\/jats:sup><\/jats:italic>. Visual responses of <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> retinal ganglion cells (RGCs) to light onset were abnormal. <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> ON RGCs were rarely recorded, but when they were, had ill\u2010defined receptive field (RF) centres and delayed onset latencies. When <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> OFF\u2010centre RGC responses were evoked by full\u2010field stimulation, significantly fewer converted that response to OFF\/ON compared to <jats:italic>Grm6<jats:sup>nob4<\/jats:sup><\/jats:italic> RGCs. <jats:italic>Grm6<jats:sup>nob4\/nob3<\/jats:sup><\/jats:italic> RGC responses verified the conclusion that the two mutants are allelic. We propose that <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> is a new model of human autosomal recessive congenital stationary night blindness. However, an allelic difference between <jats:italic>Grm6<jats:sup>nob3<\/jats:sup><\/jats:italic> and <jats:italic>Grm6<jats:sup>nob4<\/jats:sup><\/jats:italic> creates a disparity in inner retinal processing. Because the localization of GRM6 is limited to bipolar cells in the On pathway, the observed difference between RGCs in these mutants is likely to arise from differences in their inputs.<\/jats:p>","DOI":"10.1113\/jphysiol.2008.157289","type":"journal-article","created":{"date-parts":[[2008,8,8]],"date-time":"2008-08-08T00:34:03Z","timestamp":1218155643000},"page":"4409-4424","source":"Crossref","is-referenced-by-count":60,"title":["Allelic variance between GRM6 mutants, <i>Grm6<sup>nob3<\/sup><\/i> and <i>Grm6<sup>nob4<\/sup><\/i> results in differences in retinal ganglion cell visual responses"],"prefix":"10.1113","volume":"586","author":[{"given":"Dennis M.","family":"Maddox","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirstan A.","family":"Vessey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary 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