{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T13:30:12Z","timestamp":1760189412934},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1982,11,1]],"date-time":"1982-11-01T00:00:00Z","timestamp":404956800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1982,11]]},"abstract":"<jats:p>1. We have studied the effects of anoxia on the recovery of neural transmission between the perforant path and the dentate granule cells in the <jats:italic>in vitro<\/jats:italic> rat hippocampal slice. There is almost no recovery of the evoked population spike following 10 min of anoxia in slices from adult rats.<\/jats:p><jats:p>2. A 2 h exposure of slices to creatine markedly improves the recovery of the population spike (80% <jats:italic>vs<\/jats:italic>. 5%). The creatine pre\u2010incubation builds up phosphocreatine levels in the slice and prevents the large fall in ATP during anoxia; ATP falls to 7\u00b79 rather than 3\u00b76 nM\/mg protein. The intracellular pH of both groups falls to the same level during anoxia.<\/jats:p><jats:p>3. If calcium concentration in the medium is reduced to 0 while magnesium concentration is raised to 10 mM during anoxia the evoked response recovers to about 65%.<\/jats:p><jats:p>4. The data suggest that an attenuation of the fall in ATP or entry of calcium during anoxia protects the tissue against irreversible transmission damage. Thus both of these factors participate in the generation of this damage. It is not yet clear if they act independently or if one acts by altering the other.<\/jats:p><jats:p>5. In the post\u2010anoxic recovery period the intracellular concentration of potassium is reduced by about 25%. However, it is still much higher than in slices that show only partial block of the evoked response when treated with ouabain. Therefore a fall in intracellular potassium 1 h after anoxia cannot explain the lack of recovery of the evoked response in adult tissue.<\/jats:p><jats:p>6. ATP levels in the post\u2010anoxic recovery period are reduced from their pre\u2010anoxic levels (9\u00b77 <jats:italic>vs<\/jats:italic>. 13\u00b79 nM\/mg protein). However when azide or antimycin A are used to directly reduce ATP to the level found 1 h after anoxia the evoked response is reduced by only about 45%. Thus the reduced post\u2010anoxic ATP levels are not sufficient to explain the loss of the evoked response in adult tissue.<\/jats:p><jats:p>7. The data show that the irreversible loss of transmission is not due to decreased cell ATP or to decreased cell K\/Na levels 1 h after the anoxic period.<\/jats:p><jats:p>8. Since creatine pre\u2010incubation protects against irreversible transmission loss this compound or one closely related to it may prove useful in attenuating irreversible brain damage <jats:italic>in situ<\/jats:italic>.<\/jats:p>","DOI":"10.1113\/jphysiol.1982.sp014424","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T07:02:05Z","timestamp":1418972525000},"page":"459-472","source":"Crossref","is-referenced-by-count":210,"title":["Mechanisms involved in irreversible anoxic damage to the <i>in vitro<\/i> rat hippocampal slice"],"prefix":"10.1113","volume":"332","author":[{"given":"Ira S.","family":"Kass","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Lipton","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1982,11]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1982.sp014424","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1982.sp014424","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,5]],"date-time":"2023-11-05T23:56:14Z","timestamp":1699228574000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1982.sp014424"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1982,11]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1982,11]]}},"alternative-id":["10.1113\/jphysiol.1982.sp014424"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1982.sp014424","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1982,11]]}}}