Gap Junctions Propagate Melanopsin-like Responses Among Retinal Ganglion Cells in a Mouse Model of a Macular Degeneration

A missense mutation, R345W, in the extracellular matrix protein Efemp1 (or Fibulin-3) causes the autosomal dominant macular degenerative disease Malattia Leventinese (Stone et al. 1999). In mice with the same mutation, we previously discovered that about twice as many retinal ganglion cells as normal display melanopsin-like responses to light: long latency, sustained duration, and persistence when rod and cone photoreceptor input has been blocked pharmacologically (wild type: 45/354 [12.7%, SD = 7.0%]; Efemp1R345W: 109/449 [24.5%, SD = 4.3%] This study was designed to determine the origin of this physiological phenotype.