Abstract
Electrical (e-) stimulation is explored in schemes to rescue the vision of blind people, e.g. those affected by Retinitis Pigmentosa (RP). We e-activated subretinally the surviving degenerated photoreceptors (d-Phrs) of the rd1 mouse (RP model) and evoked visual responses in the blind retina. The e-stimulation was applied with a single platinum/iridium electrode. The d-Phrs (calcium-imaging) and ganglion cells (GC) activity (MEA-recording) were recorded in simultaneous multilayer recordings. The findings of this study confirm that the d-Phrs responded to e-stimulation and modulated the retinal network-activity. The application of blockers revealed that the synaptic interactions were dependent on voltage-gated calcium channels and mediated by the transmitters glutamate and GABA. Moreover, the gap junctions coupled networks promoted the lateral-spread of the e-evoked activity in the outer (~60 µm) and inner (~120 µm) retina. The activated GCs were identified as subtypes of the ON, OFF and ON-OFF classes. In conclusion, d-Phrs are the ideal interface partners for implants to elicit enhanced visual responses at higher temporal and spatial resolution. Furthermore, the retina’s intact circuity at the onset of complete blindness makes it a tempting target when considering the implantation of implants into young patients to provide a seamless transition from blinding to chip-aided vision.
Highlights
Millions of people worldwide have lost their eyesight due to hereditary, blinding diseases
The compositions of the network mediated retinal signalling were identified as glutamatergic and GABAergic for vertical retina signalling while the gap junctional (GJ) cell coupling was responsible for the lateral retinal signalling in the outer and inner retina, which was revealed by antagonising each signalling pathway with respective pharmaceutical drugs
In the rd[1] mouse model of human Retinitis Pigmentosa (RP), rod-dystrophy leads to secondary cone degeneration[16]
Summary
Millions of people worldwide have lost their eyesight due to hereditary, blinding diseases. The subretinal implant has been beneficial for blind patients in clinical trials by providing visual sensations for daily-life activities[7]. Despite this pioneering success, the implant technology faces two different types of problems: (1) Poor temporal and spatial resolution, due to the retinal implant’s technical capability (e.g. 1500 electrodes each 50 × 50 μm[10] and (2) the trial participants’ degree of retinal degeneration (e.g. blind for decades[7]). Using e-implants at the onset of the RP-dependent, complete blindness, by employing single microelectrodes e-stimulating subretinally the blind retina of the rd1 × HR2.1:TN-XL mouse model. The low d-Phrs e-activation values permit the use of denser electrode fields, featuring smaller e-stimulation electrodes, and thereby improve the performance of the subretinal implants in terms of spatial and temporal resolution
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