title: Retarded outer segment development in TrkB knockout mouse retina organ culture.
abstract: OBJECTIVE
  To determine the effects of trkB deficiency in the mouse retina on photoreceptor development and retinal organization, in the absence of confounding systemic effects.
  
  
  METHODS
  Newborn mice that carried two null trkB alleles (trkB-/-) and their wild type (WT) littermates were used for retinal organ cultures. On Day 21, rod development was assessed histologically in plastic sections (outer segment length) and retinal organization was analyzed using retinal cell-type specific antibodies. Anatomical data obtained from the organ cultures were compared to previously published histological results from in vivo data.
  
  
  RESULTS
  (1) Rod outer segment length was significantly shorter in retinas from trkB-/- mice in the presence of normal numbers of rods. (2) No dopaminergic amacrine cells were observed in the knockout retina. (3) Unlike in the in vivo condition, recoverin-positive OFF-cone bipolar cells were present in trkB-/- retinas grown in culture.
  
  
  CONCLUSIONS
  (1) These results demonstrate that rod outer segment development is compromised in the absence of trkB in the retina. (2) This study further supports our previous conclusion that the elimination of trkB expression alters rod development, because the presence of trkB receptors within the retina is essential for normal rod maturation and not because of confounding systemic effects. (3) More generally, this study stresses the importance of investigating complex phenotypes in gene knockout mice under conditions that isolate the organ under investigation from unrelated systemic variations.
authors.affiliation: Department of Ophthalmology, Medical University of South Carolina, Charleston, SC 29425, USA. rohrer@musc.edu
authors.forename: Baerbel
authors.initials: B
authors.lastname: Rohrer
authors.forename: Judith Mosinger
authors.initials: JM
authors.lastname: Ogilvie
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015415:Biomarkers / Q000032:analysis; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002454:Cell Differentiation; D002465:Cell Movement; D005136:Eye Proteins; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D051597:Hippocalcin; D007124:Immunoenzyme Techniques; D008074:Lipoproteins; D051379:Mice; D018345:Mice, Knockout / Q000235:genetics; D009419:Nerve Tissue Proteins; D009924:Organ Culture Techniques; D020813:Receptor, trkB / Q000502:physiology*; D051603:Recoverin; D012160:Retina / Q000254:growth & development; D012243:Rhodopsin / Q000378:metabolism; D012374:Rod Cell Outer Segment / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D015415:Biomarkers; D064026:Calbindins; D002135:Calcium-Binding Proteins; D005136:Eye Proteins; D005904:Glial Fibrillary Acidic Protein; D008074:Lipoproteins; D009419:Nerve Tissue Proteins; C496732:Rcvrn protein, mouse; D064030:S100 Calcium Binding Protein G; D051603:Recoverin; D051597:Hippocalcin; D012243:Rhodopsin; D014446:Tyrosine 3-Monooxygenase; D020813:Receptor, trkB