The retina in young P23H retinitis pigmentosa mice overexpresses critical components of synaptic transmission
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ABSTRACT: Homeostatic plasticity in the retina has been demonstrated using an established mouse model of Retinitis Pigmentosa caused by the P23H mutation in rhodopsin. While signaling between the sensory rod photoreceptors and rod bipolar cells is potentiated in the P23H/Gnat2-/- mice, the molecular mechanisms of homeostatic plasticity in the retina’s ribbon synapses have remained largely unknown. Furthermore, little data exists whether homeostatic plasticity occurs primarily in the presynaptic (rods) or postsynaptic (RBC) site, or both. We investigated these issues by using scRNA-seq, immunohistochemistry, and bulk retina proteomics. We show that critical components of synaptic transmission, such as SNARE complex proteins, are overexpressed in rod synaptic terminals. Additionally, we found upregulation of transsynaptic complex proteins that are relevant in the rod-RBC synapse. These results suggest that the primary homeostatic plasticity mechanism in P23H/Gnat2-/-mouse rod-RBC synapse is presynaptic scaling, but postsynaptic scaling at the RBC dendrites could also play a role in maintaining the signal transfer at the rod-RBC synapse during photoreceptor degenerative disease.
ORGANISM(S): Mus Musculus
SUBMITTER:
Ahmed Montaser
PROVIDER: PXD060180 | panorama | Mon Dec 08 00:00:00 GMT 2025
REPOSITORIES: PanoramaPublic
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