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M. Sen, B. Trexler; Light Responses and Dark Noise of AII Amacrine Cells in Rabbit Retina Slices. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4910.
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© ARVO (1962-2015); The Authors (2016-present)
AII amacrine cells receive glutamatergic inputs from rod bipolar cells (RBP) and OFF cone bipolar cells (OFFCB). In the dark, OFFCBs are depolarized and release glutamate, which might contribute to the dark noise. Noise in AII amacrine cells would diminish their sensitivity to threshold level rod signals. Therefore we sought to determine the source of the dark noise of AII amacrine cells.
Whole cell patch clamping was performed on dark adapted rabbit retina slices. Drugs were perfused using a puffer pipette. We used L-APB to block depolarizing bipolar cell light responses and NBQX to block AMPA/Kainate receptors.
NBQX substantially reduced the dark noise of AIIs and abolished the dark adapted light response. This was expected as synaptic transmission between RBP or OFFCB and AIIs is abolished in NBQX. Surprisingly, L-APB also substantially diminished the dark noise of AII amacrine cell, suggesting that it caused a decrease in glutamate release from RBP. L-APB also eliminated the dark adapted light response, as expected. Due to dark noise, AII threshold responses are only visible in averages of several flash presentations.
Our data suggest that in the slice preparation, rod bipolar cells release glutamate constitutively in the dark, generating dark noise in AII amacrine cells. If the dark noise in AIIs is also present in cone bipolar cells, ganglion cells would have to discriminate true photoisomerization events by integrating the inputs from several of their presynaptic bipolar cells. Whether AII dark noise persists in whole mount (intact) retina, where damage to photoreceptors is minimized, remains to be determined.
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