Compensatory responses to glaucoma pathology in the dorsolateral geniculate nucleus.

Shaylah McCool, Arnav Jain, Jennie C Smith, Victoria Schaal, Gurudutt Pendyala, Sowmya Yelamanchili, Matthew J Van Hook

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In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

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2 · The registry

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Shaylah McCoolDepartment of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Arnav JainDepartment of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Jennie C SmithDepartment of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Victoria SchaalDepartment of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Gurudutt PendyalaDepartment of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Sowmya YelamanchiliDepartment of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Matthew J Van HookDepartment of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

molecular neurosciencepathologysensory neuroscience

Identifiers

PMID41858631

DOI10.1016/j.isci.2026.115176

PMCPMC12995702

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LicenceCC BY-NC-ND

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.