NON-VISUAL EVOKED LFP RESPONSES IN PRIMARY VISUAL CORTEX AND SUPERIOR COLLICULUS IN <EM>RD10</EM> MICE
Forschungszentrum Jülich
Presentation
Date TBA
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Poster Board
PS04-08PM-501
Poster
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Retinitis pigmentosa causes progressive photoreceptor degeneration and ultimate blindness, depriving central visual circuits of their normal input. Because successful therapeutical vision restoration depends on the functional integrity of downstream circuits, it is critical to determine how retinal degeneration reshapes activity in major cortical and subcortical visual structures.
While previous studies of spiking activity suggested that non-visual responsiveness remains largely stable in rd10 mice, we hypothesized that Local Field Potentials (LFPs), reflecting integrated synaptic inputs and population synchrony, might reveal circuit-level alterations not captured by single-unit outputs. Here, we investigated the integrity of these pathways by analyzing non-visual evoked LFPs recorded with high-density Neuropixels probes in the primary visual cortex (V1) and superior colliculus (SC) of awake, completely blind rd10 and age-matched wild-type mice. By extracting pulse-locked Event-Related Potentials (ERPs), we quantified a variety of parameters to characterize the magnitude and temporal dynamics of the responses, including peak amplitudes, latencies, integrated response magnitude (AUC), and response duration (FWHM) following tactile (whisker deflection) and auditory (broadband click) stimulation.
Contrary to the hypothesis of generalized cross-modal plasticity, rd10 mice exhibited marked attenuation of tactile-evoked responses in both V1 and SC, accompanied by shifts in response timing. Conversely, auditory-evoked responses were largely preserved in SC, with only modest reductions in V1. These findings reveal modality- and region-specific alterations in population activity within central visual pathways following retinal degeneration. Our results highlight specific physiological constraints that may impact the efficacy of sensory reactivation in the brain upon retinal degeneration.
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