{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T05:10:36Z","timestamp":1778217036515,"version":"3.51.4"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Physiol."],"abstract":"<jats:p>Exercise has been extensively studied in Parkinson\u2019s Disease, with a particular focus on the potential for neuroprotection that has been demonstrated in animal models. While this preclinical work has provided insight into the underlying molecular mechanisms, it has not addressed the neurophysiological changes during exercise. Here, first, we tested for neuroprotective effects of adaptive wheel running exercise in the 6-hydroxydopamine mouse model of Parkinson\u2019s disease, assessing for dopamine cell preservation. Finding none, despite running performance that equaled the pre-parkinsonian state, we probed the neurophysiology of running exercise as a transient state of high motor function amidst an unameliorated Parkinsonian lesion. Exercise was associated with characteristic, excitatory changes in the dopamine-depleted substantia nigra, which could be suppressed along with running itself by dopamine receptor blockade. Going forward, the functional state evoked by exercise merits further study, as it has parallels in human disease and may represent an optimal physiologic target for neuromodulation.<\/jats:p>","DOI":"10.3389\/fphys.2026.1796624","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T04:31:38Z","timestamp":1778214698000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Exercise evokes retained motor performance without neuroprotection in a mouse model of Parkinson\u2019s disease"],"prefix":"10.3389","volume":"17","author":[{"given":"Henry M.","family":"Skelton","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]},{"name":"Department of Biomedical Engineering, Georgia Institute of Technology","place":["Atlanta, GA, United States"]},{"name":"Morehouse School of Medicine","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nathaniel","family":"Hyman","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alejandra M.","family":"Fernandez","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]},{"name":"Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center","place":["Amarillo, TX, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emma","family":"Acerbo","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madison","family":"Scott","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Georgia Institute of Technology","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ken","family":"Berglund","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claire-Anne","family":"Gutekunst","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert E.","family":"Gross","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Emory University","place":["Atlanta, GA, United States"]},{"name":"Department of Biomedical Engineering, Georgia Institute of Technology","place":["Atlanta, GA, United States"]},{"name":"Department of Neurosurgery, Rutgers Robert Wood Johnson Medical School","place":["New Brunswick, NJ, United States"]},{"name":"Department of Neurosurgery, Rutgers New Jersey Medical School","place":["Newark, NJ, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,8]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"64","DOI":"10.1007\/s11064-015-1709-8","article-title":"Moderate-intensity physical exercise protects against experimental 6-hydroxydopamine-induced hemiparkinsonism through Nrf2-antioxidant response element pathway","volume":"41","author":"Aguiar","year":"2016","journal-title":"Neurochem. 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