{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T11:25:18Z","timestamp":1789730718312,"version":"4.0.1"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,5,12]],"date-time":"2025-05-12T00:00:00Z","timestamp":1747008000000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Retinal ischemia is a significant pathological condition that contributes to visual impairment and neuronal cell death in various retinopathies. Evidence suggests that GABA release during ischemic events may exhibit neuroprotective properties, but conflicting findings highlight a potential shift in its effects due to altered chloride ion homeostasis. This study aimed to investigate the role of the GABAergic system in retinal ischemia, focusing on the temporal dynamics of GABA release and its impact on retinal damage. We hypothesized that ischemia\u2010induced changes in GABA transport and chloride ion equilibrium contribute to neuronal damage, which can be mitigated by modulating GABAergic activity. Using an ex\u00a0vivo chick retina model subjected to oxygen and glucose deprivation (OGD), during different times, we assessed morphological changes, cell death, GABA levels, transporter activity, and the levels of chloride cotransporters NKCC1 and KCC2. Pharmacological interventions, including picrotoxin and bumetanide, were used to evaluate neuroprotective effects. Our results revealed that OGD\u2010induced significant morphological changes and cell death in the retina. GABA levels were reduced in a GAT\u20101\u2010dependent manner, while picrotoxin and bumetanide demonstrated neuroprotective effects by mitigating retinal swelling and modulating the GABAergic system. Notably, OGD increased NKCC1 content, but not KCC2 levels, indicating a disruption in chloride homeostasis. These findings suggest that ischemia\u2010induced alterations in GABAergic activity and chloride transport contribute to retinal damage. Targeting these pathways with pharmacological agents, such as bumetanide, may offer therapeutic strategies for mitigating ischemic retinal injury. Further research is recommended to explore the clinical applicability of these findings in the ischemic retina.<\/jats:p>","DOI":"10.1002\/jnr.70043","type":"journal-article","created":{"date-parts":[[2025,5,12]],"date-time":"2025-05-12T06:50:02Z","timestamp":1747032602000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Modulation of\n                    <scp>GABAergic<\/scp>\n                    System in a Chicken Retinal Ischemic Model: The Role of Chloride Cotransporters"],"prefix":"10.1002","volume":"103","author":[{"given":"A. A.","family":"Nascimento","sequence":"first","affiliation":[{"name":"Laboratory Neurobiology of the Retina, Department of Neurobiology and Program of Neurosciences, Biology Institute Fluminense Federal University  Rio de Janeiro Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V. 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