The rd10 mouse is a widely used model for degenerative retinal diseases such as retinitis pigmentosa (RP). Its retina shows rhythmic spontaneous activity at a frequency of three to seven Hz, and the retinal ganglion cells (RGCs) are less electrically excitable. We hypothesize that the electrical excitability can be improved by suppressing the oscillations using the neuroprotective drugs 2-aminoethanesulphonic acid (taurine), brimonidine and betaxolol. These are involved in calcium homeostasis and may play a crucial role in neuroprotection and excitotoxicity by preventing Ca overload. Spontaneous activity and responses to electrical stimulation of isolated retinas from 3- to 4-month-old rd10 mice were recorded using multielectrode arrays. At defined times, the neuroprotectants were repeatedly added to the medium according to a standardized protocol to analyze the reproducibility and reversibility of their effects. Taurine and betaxolol significantly reduced oscillations and bursting behavior and ameliorated electrical efficiency. Brimonidine only reduced the frequency of oscillations. The effects on oscillation, spontaneous firing frequency, bursting behavior and stimulation efficiency were reproducible and reversible. The drugs tested appear to be promising therapeutic candidates for improving the residual function of RGCs. They will be further investigated and combined with other RP treatments, such as retinal prostheses, in the future.