ArticleThe Journal of physiology2025
Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell.
Article in The Journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Transient functional preservation precedes retinal ganglion cell degeneration following optic nerve crush.IBRO neuroscience reports · 2026Article
- Overexpression or Activation of Potassium Channel TASK-3 Protects Retinal Ganglion Cells and Restores Visual Function in Optic Nerve Crush.Investigative ophthalmology & visual science · 2026Article
- Gap junction protein connexin 36 proteostatic mechanisms in photoreceptor cells subjected to excitotoxic stress.Acta biochimica Polonica · 2026Article
- Cellular-resolution OCT reveals layer-specific retinal mosaics and ganglion cell degeneration in mouse retinaNeurophotonics · 2026Article
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Authors and funding
3 authors.
Funding
Abstract
Retinal ganglion cells (RGCs) are the sole output neurons of the retina and convey visual information to the brain via their axons in the optic nerve. Following injury to the optic nerve, RGC axons degenerate and many cells die. For example, a model of axon injury, the optic nerve crush (ONC), kills ∼80% of RGCs after 2 weeks. Surviving cells are biased towards 'resilient' types, including several with sustained firing to light stimulation. RGC survival may depend on activity, and there is limited understanding of how or why activity changes following optic nerve injury. Here we quantified the electrophysiological properties of a highly resilient RGC type, the sustained ON-Alpha (AlphaONS) RGC, 7 days after ONC with extracellular and whole-cell patch clamp recording. Both light- and current-driven firing were reduced after ONC, but synaptic inputs were largely intact. Resting membrane potential and input resistance were relatively unchanged, while voltage-gated currents were impaired, including a reduction in voltage-gated sodium channel current and channel density in the axon initial segment. Hyperpolarization or chelation of intracellular calcium partially rescued firing rates. Extracellular recordings at 3 days following ONC showed normal light-evoked firing from AlphaONS RGCs and other Alpha RGCs, including susceptible types. These data suggest that an injured resilient RGC reduces its activity by 1 week after injury as a consequence of reduced voltage-gated current and downregulation of intrinsic excitability via a Ca
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