title: Brn3a and Brn3b knockout mice display unvaried retinal fine structure despite major morphological and numerical alterations of ganglion cells.
abstract: Ganglion cells (GCs), the retinal output neurons, receive synaptic inputs from bipolar and amacrine cells in the inner plexiform layer (IPL) and send information to the brain nuclei via the optic nerve. Although GCs constitute less than 1% of the total retinal cells, they occur in numerous types and are the first neurons formed during retinal development. Using Brn3a and Brn3b mutant mice in which the alkaline phosphatase gene was knocked-in (Badea et al. [Neuron] 2009;61:852-864; Badea and Nathans [Vision Res] 2011;51:269-279), we studied the general effects after gene removal on the retinal neuropil together with the consequences of lack of development of large numbers of GCs onto the remaining retinal neurons of the same class. We analyzed the morphology, number, and general architecture of various neuronal types presynaptic to GCs, searching for changes secondary to the decrement in the number of their postsynaptic partners, as well as the morphology and distribution of retinal astrocytes, for their strong topographical relation to GCs. We found that, despite GC losses, retinal organization in Brn3 null mice is remarkably similar to that of wild-type controls. J. Comp. Neurol. 527:187-211, 2019. © 2016 Wiley Periodicals, Inc.
authors.affiliation: Neuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.|Retinal CIrcuit Development & Genetics Unit, Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, 20892.|Babeş Bolyai University, 400084, Cluj Napoca, Romania.
authors.forename: Miruna Georgiana
authors.initials: MG
authors.lastname: Ghinia
authors.affiliation: Neuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.
authors.forename: Elena
authors.initials: E
authors.lastname: Novelli
authors.affiliation: Retinal CIrcuit Development & Genetics Unit, Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, 20892.
authors.forename: Szilard
authors.initials: S
authors.lastname: Sajgo
authors.affiliation: Retinal CIrcuit Development & Genetics Unit, Neurobiology-Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, 20892.
authors.forename: Tudor Constantin
authors.initials: TC
authors.lastname: Badea
authors.affiliation: Neuroscience Institute of the Italian National Research Council, Pisa Research Campus, 56124, Pisa, Italy.
authors.forename: Enrica
authors.initials: E
authors.lastname: Strettoi
mesh_terms: D000818:Animals; D018398:Homeodomain Proteins; D051379:Mice; D018345:Mice, Knockout; D012160:Retina / Q000166:cytology* / Q000378:metabolism / Q000648:ultrastructure; D012165:Retinal Ganglion Cells / Q000166:cytology* / Q000378:metabolism / Q000648:ultrastructure; D050819:Transcription Factor Brn-3A / Q000172:deficiency*; D050820:Transcription Factor Brn-3B / Q000172:deficiency*
chemical_list: D018398:Homeodomain Proteins; C494189:Pou4f1 protein, mouse; C085559:Pou4f2 protein, mouse; D050819:Transcription Factor Brn-3A; D050820:Transcription Factor Brn-3B
keywords: AB_10000340; AB_10013783; AB_2079751; AB_2278725; AB_2314052; AB_2492226; AB_2533912; AB_390204; AB_399431; AB_477035; AB_477345; Brn3 transcription factors; RRIDs: AB_94166; ganglion cells; inner plexiform layer; mosaics; synapses