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Neural Circuits"],"abstract":"<jats:p>\n                    Excitotoxicity is one of the primary mechanisms of cell loss in a variety of diseases of the central and peripheral nervous systems. Other than the previously established signaling pathways of excitotoxicity, which depend on the excessive release of glutamate from axon terminals or over-activation of NMDA receptors (NMDARs), Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx-triggered excitotoxicity through Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -permeable (CP)-AMPA receptors (AMPARs) is detected in multiple disease models. In this review, both acute brain insults (e.g., brain trauma or spinal cord injury, ischemia) and chronic neurological disorders, including Epilepsy\/Seizures, Huntington\u2019s disease (HD), Parkinson\u2019s disease (PD), Alzheimer\u2019s disease (AD), amyotrophic lateral sclerosis (ALS), chronic pain, and glaucoma, are discussed regarding the CP-AMPAR-mediated excitotoxicity. Considering the low expression or absence of CP-AMPARs in most cells, specific manipulation of the CP-AMPARs might be a more plausible strategy to delay the onset and progression of pathological alterations with fewer side effects than blocking NMDARs.\n                  <\/jats:p>","DOI":"10.3389\/fncir.2021.711564","type":"journal-article","created":{"date-parts":[[2021,8,17]],"date-time":"2021-08-17T08:58:28Z","timestamp":1629190708000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":173,"title":["Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders"],"prefix":"10.3389","volume":"15","author":[{"given":"Changyong","family":"Guo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao-Ying","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,8,17]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"75","DOI":"10.1007\/s00401-010-0678-x","article-title":"TDP-43 pathology in sporadic ALS occurs in motor neurons lacking the RNA editing enzyme ADAR2","volume":"120","author":"Aizawa","year":"2010","journal-title":"Acta Neuropathol."},{"key":"B2","doi-asserted-by":"publisher","first-page":"446","DOI":"10.1007\/s13311-020-00840-7","article-title":"Cell death and recovery in traumatic brain injury","volume":"17","author":"Akamatsu","year":"2020","journal-title":"Neurotherapeutics"},{"key":"B3","doi-asserted-by":"publisher","first-page":"297","DOI":"10.1016\/0006-8993(95)00922-d","article-title":"Editing for an AMPA receptor subunit RNA in prefrontal cortex and striatum in Alzheimer\u2019s disease, Huntington\u2019s disease and schizophrenia","volume":"699","author":"Akbarian","year":"1995","journal-title":"Brain Res."},{"key":"B4","doi-asserted-by":"publisher","first-page":"152","DOI":"10.1016\/j.preteyeres.2011.11.002","article-title":"The molecular basis of retinal ganglion cell death in glaucoma","volume":"31","author":"Almasieh","year":"2012","journal-title":"Prog. 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