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In the widely used mouse model of retinal degeneration,  rd1,  the loss of photoreceptors leads to rhythmic electrical activity of around 10–16 Hz in the remaining retinal network. Recent studies suggest that this oscillation is formed within the electrically coupled network of AII amacrine cells and ON-bipolar cells. A second mouse model,  rd10 , displays a delayed onset and slower progression of degeneration, making this mouse strain a better model for human retinitis pigmentosa. In  rd10 , oscillations occur at a frequency of 3–7 Hz, raising the question whether oscillations have the same origin in the two mouse models. As  rd10  is increasingly being used as a model to develop experimental therapies, it is important to understand the mechanisms underlying the spontaneous rhythmic activity. To study the properties of oscillations in  rd10  retina we combined multi electrode recordings with pharmacological manipulation of the retinal network. Oscillations were abolished by blockers for ionotropic glutamate receptors and gap junctions. Frequency and amplitude of oscillations were modulated strongly by blockers of inhibitory receptors and to a lesser extent by blockers of HCN channels. In summary, although we found certain differences in the pharmacological modulation of rhythmic activity in  rd10  compared to  rd1 , the overall pattern looked similar. This suggests that the generation of rhythmic activity may underlie similar mechanisms in  rd1  and  rd10  retina.

Pharmacological Analysis of Intrinsic Neuronal Oscillations in rd10 Retina