University of Louisville
Retinal Ganglion Cell Dendritic Stratification of the nob2 Mouse
Institution
University of Louisville
Faculty Advisor/ Mentor
Ron Gregg
Abstract
Light dependent activity within the retina is required for normal retinal ganglion cell (RGC) dendritic stratification into ON and OFF sub-laminae. The first synapse in this pathway is dependent on the expression and normal function of the Cav1.4 voltage dependent calcium channel (VDCC). The pore-forming (α1F) subunit of the VDCC is encoded by the CACNA1F gene. Mutations in this gene cause incomplete congenital stationary night blindness (CSNB2) in humans, and a naturally occurring mouse model of CSNB2 has been identified and named nob2. This study investigates whether the abnormal photoreceptor to bipolar cell transmission in the nob2 mouse alters RGC dendritic stratification in the inner plexiform layer (IPL). Transgenic mice expressing yellow fluorescent protein (YFP) in a small fraction of RGCs were crossed with nob2 mice and immunohistochemical techniques were used to determine the dendritic stratification of these RGCs. Antibodies to YFP and Choline acetyltransferase (ChAT) were used to identify the ON and OFF sub-lamina of the IPL. The results of this study reveal no differences in the dendritic stratification of RGCs in nob2 mice. RGC stratification appears to proceed normally despite the loss of normal signaling from the photoreceptors to bipolar cells and loss of α1F subunit expression within the retina.
Retinal Ganglion Cell Dendritic Stratification of the nob2 Mouse
Light dependent activity within the retina is required for normal retinal ganglion cell (RGC) dendritic stratification into ON and OFF sub-laminae. The first synapse in this pathway is dependent on the expression and normal function of the Cav1.4 voltage dependent calcium channel (VDCC). The pore-forming (α1F) subunit of the VDCC is encoded by the CACNA1F gene. Mutations in this gene cause incomplete congenital stationary night blindness (CSNB2) in humans, and a naturally occurring mouse model of CSNB2 has been identified and named nob2. This study investigates whether the abnormal photoreceptor to bipolar cell transmission in the nob2 mouse alters RGC dendritic stratification in the inner plexiform layer (IPL). Transgenic mice expressing yellow fluorescent protein (YFP) in a small fraction of RGCs were crossed with nob2 mice and immunohistochemical techniques were used to determine the dendritic stratification of these RGCs. Antibodies to YFP and Choline acetyltransferase (ChAT) were used to identify the ON and OFF sub-lamina of the IPL. The results of this study reveal no differences in the dendritic stratification of RGCs in nob2 mice. RGC stratification appears to proceed normally despite the loss of normal signaling from the photoreceptors to bipolar cells and loss of α1F subunit expression within the retina.