{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T19:21:54Z","timestamp":1790882514896,"version":"4.1.0"},"reference-count":69,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2022,10,3]],"date-time":"2022-10-03T00:00:00Z","timestamp":1664755200000},"content-version":"vor","delay-in-days":32,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Stanley Cohen Innovation Fund"},{"DOI":"10.13039\/100006312","name":"BrightFocus Foundation","doi-asserted-by":"crossref","award":["G2022011S"],"award-info":[{"award-number":["G2022011S"]}],"id":[{"id":"10.13039\/100006312","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Potocsnak Family Vision Research Center Fund"},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["EY017427"],"award-info":[{"award-number":["EY017427"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["EY024997"],"award-info":[{"award-number":["EY024997"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["EY008126"],"award-info":[{"award-number":["EY008126"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH","award":["CA68485"],"award-info":[{"award-number":["CA68485"]}]},{"name":"NIH","award":["DK20593"],"award-info":[{"award-number":["DK20593"]}]},{"name":"NIH","award":["DK58404"],"award-info":[{"award-number":["DK58404"]}]},{"name":"NIH","award":["DK59637"],"award-info":[{"award-number":["DK59637"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Optic neuropathies are characterized by degeneration of retinal ganglion cell axonal projections to the brain, including acute conditions like optic nerve trauma and progressive conditions such as glaucoma. Despite different aetiologies, retinal ganglion cell axon degeneration in traumatic optic neuropathy and glaucoma share common pathological signatures. We compared how early pathogenesis of optic nerve trauma and glaucoma influence axon function in the mouse optic projection. We assessed pathology by measuring anterograde axonal transport from retina to superior colliculus, current-evoked optic nerve compound action potential and retinal ganglion cell density 1 week following unilateral optic nerve crush or intraocular pressure elevation. Nerve crush reduced axon transport, compound axon potential and retinal ganglion cell density, which were unaffected by intraocular pressure elevation. Surprisingly, optic nerves contralateral to crush demonstrated 5-fold enhanced excitability in compound action potential compared with na\u00efve nerves. Enhanced excitability in contralateral sham nerves is not due to increased accumulation of voltage-gated sodium channel 1.6, or ectopic voltage-gated sodium channel 1.2 expression within nodes of Ranvier. Our results indicate hyperexcitability is driven by intrinsic responses of \u03b1ON-sustained retinal ganglion cells. We found \u03b1ON-sustained retinal ganglion cells in contralateral, sham and eyes demonstrated increased responses to depolarizing currents compared with those from na\u00efve eyes, while light-driven responses remained intact. Dendritic arbours of \u03b1ON-sustained retinal ganglion cells of the sham eye were like na\u00efve, but soma area and non-phosphorylated neurofilament H increased. Current- and light-evoked responses of sham \u03b1OFF-sustained retinal ganglion cells remained stable along with somato-dendritic morphologies. In retinas directly affected by crush, light responses of \u03b1ON- and \u03b1OFF-sustained retinal ganglion cells diminished compared with na\u00efve cells along with decreased dendritic field area or branch points. Like light responses, \u03b1OFF-sustained retinal ganglion cell current-evoked responses diminished, but surprisingly, \u03b1ON-sustained retinal ganglion cell responses were similar to those from na\u00efve retinas. Optic nerve crush reduced dendritic length and area in \u03b1ON-sustained retinal ganglion cells in eyes ipsilateral to injury, while crush significantly reduced dendritic branching in \u03b1OFF-sustained retinal ganglion cells. Interestingly, 1 week of intraocular pressure elevation only affected \u03b1OFF-sustained retinal ganglion cell physiology, depolarizing resting membrane potential in cells of affected eyes and blunting current-evoked responses in cells of saline-injected eyes. Collectively, our results suggest that neither saline nor sham surgery provide a true control, chronic versus acute optic neuropathies differentially affect retinal ganglion cells composing the ON and OFF pathways, and acute stress can have near-term effects on the contralateral projection.<\/jats:p>","DOI":"10.1093\/braincomms\/fcac251","type":"journal-article","created":{"date-parts":[[2022,10,1]],"date-time":"2022-10-01T12:22:04Z","timestamp":1664626924000},"source":"Crossref","is-referenced-by-count":10,"title":["Axon hyperexcitability in the contralateral projection following unilateral optic nerve crush in mice"],"prefix":"10.1093","volume":"4","author":[{"given":"Nolan R","family":"McGrady","sequence":"first","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph M","family":"Holden","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcio","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M","family":"Boal","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael L","family":"Risner","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J","family":"Calkins","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology and Visual Sciences, Vanderbilt Eye Institute, Vanderbilt University Medical Center , AA7103 MCN\/VUIIS, 1161 21st Ave. S., Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2022,10,3]]},"reference":[{"key":"2022101718164377200_fcac251-B1","doi-asserted-by":"crossref","first-page":"720","DOI":"10.1002\/ana.21390","article-title":"Spreading depolarizations occur in human ischemic stroke with high incidence","volume":"63","author":"Dohmen","year":"2008","journal-title":"Ann 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