{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T15:21:07Z","timestamp":1777648867235,"version":"3.51.4"},"reference-count":52,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,11,24]],"date-time":"2015-11-24T00:00:00Z","timestamp":1448323200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100009123","name":"Norges Teknisk-Naturvitenskapelige Universitet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100009123","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Mitochondrial impairment is a key feature underlying neonatal hypoxic\u2010ischemic (HI) brain injury and melatonin is potentially neuroprotective through its effects on mitochondria. In this study, we have used <jats:sup>1<\/jats:sup>H and <jats:sup>13<\/jats:sup>C NMR spectroscopy after injection of [1\u2010<jats:sup>13<\/jats:sup>C]glucose and [1,2\u2010<jats:sup>13<\/jats:sup>C]acetate to examine neuronal and astrocytic metabolism in the early reperfusion phase after unilateral HI brain injury in 7\u2010day\u2010old rat pups, exploring the effects of HI on mitochondrial function and the potential protective effects of melatonin on brain metabolism. One hour after hypoxia\u2010ischemia, astrocytic metabolism was recovered and glycolysis was normalized, whereas mitochondrial metabolism in neurons was clearly impaired. Pyruvate carboxylation was also lower in both hemispheres after HI. The transfer of glutamate from neurons to astrocytes was higher whereas the transfer of glutamine from astrocytes to neurons was lower 1\u00a0h after HI in the contralateral hemisphere. Neuronal metabolism was equally affected in pups treated with melatonin (10\u00a0mg\/kg) immediately after HI as in vehicle treated pups indicating that the given dose of melatonin was not capable of protecting the neuronal mitochondria in this early phase after HI brain injury. However, any beneficial effects of melatonin might have been masked by modulatory effects of the solvent dimethyl sulfoxide on cerebral metabolism.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13420-fig-0004-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\nNeuronal and astrocytic metabolism was examined by <jats:sup>13<\/jats:sup>C and <jats:sup>1<\/jats:sup>H NMR spectroscopy in the early reperfusion phase after unilateral hypoxic\u2010ischemic brain injury and melatonin treatment in neonatal rats. One hour after hypoxia\u2010ischemia astrocytic mitochondrial metabolism had recovered and glycolysis was normalized, whereas mitochondrial metabolism in neurons was impaired. Melatonin treatment did not show a protective effect on neuronal metabolism.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.13420","type":"journal-article","created":{"date-parts":[[2015,11,3]],"date-time":"2015-11-03T07:59:34Z","timestamp":1446537574000},"page":"339-350","source":"Crossref","is-referenced-by-count":20,"title":["No improvement of neuronal metabolism in the reperfusion phase with melatonin treatment after hypoxic\u2010ischemic brain injury in the neonatal rat"],"prefix":"10.1111","volume":"136","author":[{"given":"Hester R.","family":"Berger","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine Children's and Women's Health Norwegian University of Science and Technology (NTNU) Trondheim Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tora Sund","family":"Morken","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Children's and Women's Health Norwegian University of Science and Technology (NTNU) Trondheim Norway"},{"name":"Department of Ophthalmology Trondheim University Hospital Trondheim Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Riyas","family":"Vettukattil","sequence":"additional","affiliation":[{"name":"Department of Circulation and Medical Imaging Norwegian University of Science and Technology (NTNU) Trondheim Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann\u2010Mari","family":"Brubakk","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Children's and Women's Health Norwegian University of Science and Technology (NTNU) Trondheim Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ursula","family":"Sonnewald","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Norwegian University of Science and Technology (NTNU) Trondheim Norway"},{"name":"Department of Drug Design and Pharmacology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marius","family":"Wider\u00f8e","sequence":"additional","affiliation":[{"name":"Department of Circulation and Medical Imaging Norwegian University of Science and Technology (NTNU) Trondheim Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,11,24]]},"reference":[{"key":"e_1_2_7_2_1","first-page":"771","article-title":"Histological study of the protective effect of melatonin on neural cells after neonatal hypoxia\u2010ischemia","volume":"27","author":"Alonso\u2010Alconada D.","year":"2012","journal-title":"Histol. 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