{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:02:17Z","timestamp":1772118137434,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2022,10,2]],"date-time":"2022-10-02T00:00:00Z","timestamp":1664668800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Sevoflurane acts as a gamma\u2010aminobutyric acid subtype A receptor agonist and can induce widespread apoptosis of immature dentate granule cells in postnatal day 21 mice. The dentate granule cells of postnatal day 21 mice undergo a developmental stage when gamma\u2010aminobutyric acid (GABA) shifts from inducing the depolarization of neurons to causing hyperpolarization. However, it is unclear whether sevoflurane induces apoptosis of immature granule cells by facilitating the depolarization or hyperpolarization of neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We utilized bumetanide, an Na\n                      <jats:sup>+<\/jats:sup>\n                      \u2013K\n                      <jats:sup>+<\/jats:sup>\n                      \u20132Cl\n                      <jats:sup>\u2212<\/jats:sup>\n                      cotransporter isoform 1 (NKCC1) antagonist, to determine whether the NKCC1\u2010mediated GABA depolarization of neurons plays a role in sevoflurane\u2010induced neuroapoptosis. We also investigated whether sevoflurane exposure is related to long\u2010term cognitive dysfunction in postnatal day 21 mice and explored the possible protective effects of bumetanide.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Bumetanide attenuated the sevoflurane\u2010induced apoptosis of dentate granule cells in postnatal day 21 mice. Exposure to sevoflurane at postnatal day 21 mice did not affect their motor ability or anxiety level, and it had no effect on spatial learning or memory functions. However, sevoflurane exposure at postnatal day 21 impaired the pattern separation ability in the contextual fear discrimination test; bumetanide mitigated this effect of sevoflurane as well.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Bumetanide attenuates sevoflurane\u2010induced apoptosis and is a promising prospect for protecting against anesthesia\u2010induced neurotoxicity in the developing brain.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.2768","type":"journal-article","created":{"date-parts":[[2022,10,3]],"date-time":"2022-10-03T00:58:29Z","timestamp":1664758709000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Bumetanide attenuates sevoflurane\u2010induced neuroapoptosis in the developing dentate gyrus and impaired behavior in the contextual fear discrimination learning 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