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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 \u223c80% of RGCs after 2\u00a0weeks. Surviving cells are biased towards \u2018resilient\u2019 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\u2010Alpha (AlphaONS) RGC, 7\u00a0days after ONC with extracellular and whole\u2010cell patch clamp recording. Both light\u2010 and current\u2010driven firing were reduced after ONC, but synaptic inputs were largely intact. Resting membrane potential and input resistance were relatively unchanged, while voltage\u2010gated currents were impaired, including a reduction in voltage\u2010gated 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\u00a0days following ONC showed normal light\u2010evoked firing from AlphaONS RGCs and other Alpha RGCs, including susceptible types. These data suggest that an injured resilient RGC reduces its activity by 1\u00a0week after injury as a consequence of reduced voltage\u2010gated current and downregulation of intrinsic excitability via a Ca\n                      <jats:sup>2+<\/jats:sup>\n                      \u2010dependent mechanism. Reduced excitability may be due to degradation of the axon but could also be energetically beneficial, preserving energy for survival and regeneration.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16573-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Retinal ganglion cell (RGC) types show diverse rates of survival after axon injury.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>A resilient RGC type (sustained ON\u2010Alpha RGC) maintains its synaptic inputs 1\u00a0week after injury.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The resilient RGC type shows diminished firing and reduced expression of axon initial segment genes 1\u00a0week after injury<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Activity deficits reflect dysfunction of intrinsic properties (Na\n                            <jats:sup>+<\/jats:sup>\n                            channels, intracellular Ca\n                            <jats:sup>2+<\/jats:sup>\n                            ), not changes to synaptic input.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Both resilient and susceptible Alpha RGC types show intact firing at 3\u00a0days after injury, suggesting that activity at this time point does not predict resilience.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp286414","type":"journal-article","created":{"date-parts":[[2025,2,22]],"date-time":"2025-02-22T13:15:01Z","timestamp":1740230101000},"page":"6623-6652","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell"],"prefix":"10.1113","volume":"603","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5559-4630","authenticated-orcid":false,"given":"Thomas 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