THE ROLE OF BDNF IN EYE-SPECIFIC PATTERNING OF VISUAL CONNECTIONS. A.W. Lyckman1*; G. Fan2; M. Rios2; R. Jaenisch2; M. Sur1 1. Dept Brain & Cognitive Sci, MIT, Cambridge, MA, USA 2. Whitehead Institute for Biomedical Research, Cambridge, MA, USA Refinement of eye-specific segregation of visual connections is thought to involve activity-dependent retraction of overlapping (binocular) inputs. Remodeling of the terminal arbors of retinal fibers in the lateral geniculate nucleus (LGN) may require brain-derived neurotrophic factor (BDNF), a neurotrophin whose expression is modulated by activity in the LGN and the visual cortex. We have asked whether eye-specific segregation of retinal inputs to the LGN occurs in the absence of BDNF using two transgenic mouse lines: BDNF-knockouts (KO), carrying a homozygous, germ-line deletion of the BDNF gene; and, brain-specific mutants (BM), in which the BDNF gene is deleted from daughter cells of CNS progenitor cells in mid-gestation. In wild type mice, eye-specific segregation in LGN is complete by P8. KO mice (examined at P16) and BM mice (examined at P11) received intraocular injections of cholera toxin B-subunit (CTB) coupled to fluorescein in one eye, and CTB coupled to tetramethylrhodamine in the other eye. The next day, mice were euthanized and transcardially perfused with 4% paraformaldehyde; vibratome sections of brain were examined by confocal microscopy. Projections from the two eyes were just as well segregated in the KO and BM mice as in their litter mate controls or wild type mice. No additional overlap between axons from the two eyes was detected in the BDNF-deficient mice. These data suggest that BDNF may not be required for refinement of eye-specific segregation in the LGN. Whether binocular overlap of thalamocortical projections is altered in BDNF-deficient mice is under examination. Supported by: EY11512 (MS) & R35 CA44339 (RJ).