• Progress in Medical Physics
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• v.19 no.1
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• pp.73-79
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• 2008

Retinal prosthesis is regarded as the most feasible method for the blind caused by retinal diseases such as retinitis pigmentosa (RP) or age related macular degeneration (AMD). Recently Korean consortium launched for developing retinal prosthesis. One of the prerequisites for the success of retinal prosthesis is the optimization of the electrical stimuli applied through the prosthesis. Since electrical characteristics of degenerate retina are expected to differ from those of normal retina, we performed voltage stimulation experiment both in normal and degenerate retina to provide a guideline for the optimization of electrical stimulation for the upcoming prosthesis. After isolation of retina, retinal patch was attached with the ganglion cell side facing the surface of microelectrode arrays (MEA). $8{\times}8$ grid layout MEA (electrode diameter: $30{\mu}m$, electrode spacing: $200{\mu}m$, and impedance: $50k{\Omega}$ at 1 kHz) was used to record in-vitro retinal ganglion cell activity. Mono-polar electrical stimulation was applied through one of the 60 MEA channel, and the remaining channels were used for recording. The electrical stimulus was a constant voltage, charge-balanced biphasic, anodic-first square wave pulse without interphase delay, and 50 trains of pulse was applied with a period of 2 sec. Different electrical stimuli were applied. First, pulse amplitude was varied (voltage: $0.5{\sim}3.0V$). Second, pulse duration was varied $(100{\sim}1,200{\mu}s)$. Evoked responses were analyzed by PSTH from averaged data with 50 trials. Charge density was calculated with Ohm's and Coulomb's law. In normal retina, by varying the pulse amplitude from 0.5 to 3V with fixed duration of $500{\mu}s$, the threshold level for reliable ganglion cell response was found at 1.5V. The calculated threshold of charge density was $2.123mC/cm^2$. By varying the pulse duration from 100 to $1,200{\mu}s$ with fixed amplitude of 2V, the threshold level was found at $300{\mu}s$. The calculated threhold of charge density was $1.698mC/cm^2$. Even after the block of ON-pathway with L-(1)-2-amino-4-phosphonobutyric acid (APB), electrical stimulus evoked ganglion cell activities. In this APB-induced degenerate retina, by varying the pulse duration from 100 to $1200{\mu}s$ with fixed voltage of 2 V, the threshold level was found at $300{\mu}s$, which is the same with normal retina. More experiment with APB-induced degenerate retina is needed to make a clear comparison of threshold of charge density between normal and degenerate retina.

• Progress in Medical Physics
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• v.19 no.3
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• pp.157-163
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• 2008

Retinal prosthesis is regarded as the most feasible method for the blind caused by retinal diseases such as retinitis pigmentosa or age-related macular degeneration. One of the prerequisites for the success of retinal prosthesis is the optimization of the electrical stimuli applied through the prosthesis. Since electrical characteristics of degenerate retina are expected to differ from those of normal retina, we investigated differences of the retinal waveforms in normal and degenerate retina to provide a guideline for the optimization of electrical stimulation for the upcoming prosthesis. After isolation of retina, retinal patch was attached with the ganglion cell side facing the surface of microelectrode arrays (MEA). $8{\times}8$ grid layout MEA (electrode diameter: $30{\mu}m$, electrode spacing: $200{\mu}m$, and impedance: 50 $k{\Omega}$ at 1 kHz) was used to record in-vitro retinal ganglion cell activity. In normal mice (C57BL/6J strain) of postnatal day 28, only short duration (<2 ms) retinal spikes were recorded. In rd/rd mice (C3H/HeJ strain), besides normal spikes, waveform with longer duration (~100 ms), the slow wave component was recorded. We attempted to understand the mechanism of this slow wave component in degenerate retina using various synaptic blockers. We suggest that stronger glutamatergic input from bipolar cell to the ganglion cell in rd/rd mouse than normal mouse contributes the most to this slow wave component. Out of many degenerative changes, we favor elimination of the inhibitory horizontal input to bipolar cells as a main contributor for a relatively stronger input from bipolar cell to ganglion cell in rd/rd mouse.