Document Type
Article
Journal Title
iScience
Publication Date
2026
Volume
29
Abstract
Glaucoma disrupts the conveyance of retinal signals to visual regions of the brain such as the dorsolateral geniculate nucleus (dLGN) due to degeneration of retinal ganglion cells (RGCs) and their axons. Although plasticity during development allows altered visual experience to modulate dLGN synapses and excitability, evidence for experience-dependent dLGN plasticity in adults is limited. However, glaucoma might trigger compensatory plasticity in adult dLGN, thereby compensating for diminished RGC synaptic drive. Here, we tested this theory using aged DBA/2J mice, which develop high intraocular pressure and glaucoma. In brain slice recordings, we found that diminished RGC inputs could drive robust action potential firing in dLGN relay neurons that was comparable to controls. This was accompanied by increased intrinsic excitability and decreased magnitude of sustained inhibitory currents from delta subunit-containing GABA receptors. These results implicate multiple cellular and synaptic mechanisms that support signaling despite the diminished RGC inputs in glaucoma.
DOI Link
ISSN
2589-0042
Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.
Recommended Citation
McCool, Shaylah; Jain, Arnav; Smith, Jennie C.; Schaal, Victoria L.; Pendyala, Gurudutt; Yelamanchili, Sowmya V.; and Van Hook, Matthew J., "Compensatory Responses to Glaucoma Pathology in the Dorsolateral Geniculate Nucleus" (2026). Journal Articles: Anesthesiology. 26.
https://digitalcommons.unmc.edu/com_anesth_articles/26