{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T10:34:53Z","timestamp":1771670093519,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,1,2]],"date-time":"2012-01-02T00:00:00Z","timestamp":1325462400000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>TRPM1 is a spontaneously active non\u2010selective cation channel that has recently been shown to play an important role in the depolarizing light responses of ON bipolar cells. Consistent with this role, mutations in the <jats:italic>TRPM1<\/jats:italic> gene have been identified as a principal cause of congenital stationary night blindness. However, previous microarray studies have shown that <jats:italic>Trpm1<\/jats:italic> and <jats:italic>Trpm3<\/jats:italic> are acutely regulated by light in the eyes of mice lacking rods and cones (<jats:italic>rd\/rd cl<\/jats:italic>), a finding consistent with a role in non\u2010image\u2010forming photoreception. In this study we show that pupillary light responses are significantly attenuated in both <jats:italic>Trpm1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and <jats:italic>Trpm3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> animals. <jats:italic>Trpm1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice exhibit a profound deficit in the pupillary response that is far in excess of that observed in mice lacking rods and cones (<jats:italic>rd\/rd cl<\/jats:italic>) or melanopsin, and cannot be explained by defects in bipolar cell function alone. Immunolocalization studies suggest that TRPM1 is expressed in ON bipolar cells and also a subset of cells in the ganglion cell layer, including melanopsin\u2010expressing photosensitive retinal ganglion cells (pRGCs). We conclude that, in addition to its role in bipolar cell signalling, TRPM1 is involved in non\u2010image\u2010forming responses to light and may perform a functional role within pRGCs. By contrast, <jats:italic>TRPM3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice display a more subtle pupillary phenotype with attenuated responses under bright light and dim light conditions. Expression of TRPM3 is detected in Muller cells and the ciliary body but is absent from pRGCs, and thus our data support an indirect role for TRPM3 in pupillary light responses.<\/jats:p>","DOI":"10.1111\/j.1460-9568.2011.07944.x","type":"journal-article","created":{"date-parts":[[2012,1,3]],"date-time":"2012-01-03T03:46:00Z","timestamp":1325562360000},"page":"34-43","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":60,"title":["Profound defects in pupillary responses to light in TRPM\u2010channel null mice: a role for TRPM channels in non\u2010image\u2010forming photoreception"],"prefix":"10.1111","volume":"35","author":[{"given":"Steven","family":"Hughes","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carina 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