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    Type 3a and type 3b OFF cone bipolar cells provide for the alternative rod pathway in the mouse retina.
        
        J. Comp. Neurol. 502, 1123-1137 (2007)
    
    
    
	    The mammalian retina provides several pathways to relay the information from the photoreceptors to the ganglion cells. Cones feed into ON and OFF cone bipolar cells that excite ON and OFF ganglion cells, respectively. In the "classical" rod pathway, rods feed into rod bipolar cells that provide input to both the ON and the OFF pathway via AII amacrine cells. Recent evidence suggests an alternative rod pathway in which rods directly contact some types of OFF cone bipolar cells. The mouse has become an important model system for retinal research. We performed an immunohistochemical analysis on the level of light and electron microscopy to identify the bipolar cells and ganglion cells that are involved in the alternative rod pathway of the mouse retina. 1) We identify a new bipolar cell type, showing that type 3 OFF cone bipolar cells comprise two distinct cell types, that we termed 3a and 3b. Type 3a cells express the ion channel HCN4. Type 3b bipolar cells represent a hitherto unknown cell type that can be identified with antibodies against the regulatory subunit RIIbeta of protein kinase A. 2) We show that both 3a and 3b cells form flat contacts at cone pedicles and rod spherules. 3) Finally, we identify an OFF ganglion cell type whose dendrites costratify with type 3a and 3b bipolar cell axon terminals. These newly identified cell types represent the basis of a neuronal circuit in the mammalian retina that could provide for an alternative fast rod pathway.
	
	
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        Publication type
        Article: Journal article
    
 
    
        Document type
        Scientific Article
    
 
     
    
    
        Keywords
        retina; bipolar cell; alternative rod pathway; immunohistochemistry
    
 
     
    
    
        Language
        english
    
 
    
        Publication Year
        2007
    
 
     
    
        HGF-reported in Year
        2007
    
 
    
    
        ISSN (print) / ISBN
        0021-9967
    
 
    
        e-ISSN
        1096-9861
    
 
    
     
     
	     
	 
	 
     
	
    
        Quellenangaben
        
	    Volume: 502,  
	    Issue: 6,  
	    Pages: 1123-1137 
	    
	    
	
    
 
    
         
        
            Publisher
            Wiley
        
 
         
	
         
         
         
         
         
	
         
         
         
    
         
         
         
         
         
         
         
    
        Reviewing status
        Peer reviewed
    
 
    
        Institute(s)
        Institute of Molecular Immunology (IMI)
    
 
     
     
    
        PSP Element(s)
        G-501700-003
    
 
     
     	
    
        PubMed ID
        17447251
    
    
    
        WOS ID
        000246386700015
    
    
        Scopus ID
        34249326586
    
    
        Erfassungsdatum
        2007-11-26