Journal Article

FZJ-2024-00741

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Electrophysiological properties of layer 2/3 pyramidal neurons in the primary visual cortex of a retinitis pigmentosa mouse model (rd10)

Halfmann, C. ; Rüland, T. ; Müller, F.FZJ* ; Jehasse, K. ; Kampa, B. M. (Corresponding author)FZJ*

2023
Frontiers Research Foundation Lausanne

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Please use a persistent id in citations: doi:10.3389/fncel.2023.1258773  doi:10.34734/FZJ-2024-00741

Abstract: Retinal degeneration is one of the main causes of visual impairment and blindness. One group of retinal degenerative diseases, leading to the loss of photoreceptors, is collectively termed retinitis pigmentosa. In this group of diseases, the remaining retina is largely spared from initial cell death making retinal ganglion cells an interesting target for vision restoration methods. However, it is unknown how downstream brain areas, in particular the visual cortex, are affected by the progression of blindness. Visual deprivation studies have shown dramatic changes in the electrophysiological properties of visual cortex neurons, but changes on a cellular level in retinitis pigmentosa have not been investigated yet. Therefore, we used the rd10 mouse model to perform patch-clamp recordings of pyramidal neurons in layer 2/3 of the primary visual cortex to screen for potential changes in electrophysiological properties resulting from retinal degeneration. Compared to wild-type C57BL/6 mice, we only found an increase in intrinsic excitability around the time point of maximal retinal degeneration. In addition, we saw an increase in the current amplitude of spontaneous putative inhibitory events after a longer progression of retinal degeneration. However, we did not observe a long-lasting shift in excitability after prolonged retinal degeneration. Together, our results provide evidence of an intact visual cortex with promising potential for future therapeutic strategies to restore vision.

Note: This study was funded by the Deutsche Forschungsgemeinschaft(DFG, German Research Foundation)−368482240/GRK2416 andGRK2610: Innoretvision.

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Contributing Institute(s):

1. Molekular- und Zellphysiologie (IBI-1)
2. Jara-Institut Brain structure-function relationships (INM-10)

Research Program(s):

1. 5241 - Molecular Information Processing in Cellular Systems (POF4-524) (POF4-524)
2. GRK 2416 - GRK 2416: MultiSenses-MultiScales: Neue Ansätze zur Aufklärung neuronaler multisensorischer Integration (368482240) (368482240)
3. GRK 2610 - GRK 2610: Innovative Schnittstellen zur Retina für optimiertes künstliches Sehen - InnoRetVision (424556709) (424556709)

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