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Ye Tao, Tao Chen, Junhui Xue, Jijing Pang, Zuoming Zhang; Visual Signal Pathway Reorganization in a Rat Model of Congenital Stationary Night Blindness (CSNB) with Cacana1f Gene Mutation. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4655.
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© ARVO (1962-2015); The Authors (2016-present)
Cacana1f gene mutation cause CSNB in mammals including human. To clarify the pathological mechanism of CSNB, we tested electrical signal transmission within inner retinal circuit after neuron remolding in Cacana1f mutant rat.
Retinas were isolated from either spontaneous Cacana1f mutant or wild type rats, and placed into the recording chamber with the ganglion cell layer facing the biochip electrode array. Then light-driven responses of the ganglion cells were recorded with a multi-electrode array system (MED-64, Panasonic, Japan). Retinas were perfused with aerated Ringer’s solution for 1 hour before recording. Measurements were performed both with and without light stimulation. Chemical compounds were bath-applied through an active perfusion system. The obtained data were further analyzed off-line.
Typical electrical responses were successfully recorded both in wild type rats and Cacana1f mutant rats. In Cacana1f mutant retinas, the light-induced a-waves had decreased amplitude but increased latency, while b-waves vanished. These responsive a-waves were not blocked by the application of 100 µM APB, 2-amino-4-phosphobutyric acid while b-waves were. A lower signal/noise(S/N) ratio caused by a increase in spontaneous firing rate and a decrease in the robustness of light-driven signaling reflects a loss in the ability of ganglion cells to encode visual signals reliably and economically. More OFF ganglion cells (off: 182 / on: 125, n=15) in Cacana1f mutant retinas and more ON ganglion cells in wild type retinas (off: 206/ on: 283, n=15) were detected during recording.
Our data suggest ON pathway is somehow disconnected from ganglion cells while OFF pathways might be preferentially selected by Cacana1f mutant retina. Dysfunction of the simultaneous photoreceptor neurotransmitter release and loss in signaling efficiency together may be the causes of CSNB phenotype, and it is not clear whether the latter are reversible.
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