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To investigate whether neonatal HIE alters neuronal activity, nociceptive behavior, and serum neuroplasticity mediators (brain\u2010derived neurotrophic factor [BDNF] and tumor necrosis factor\u2010\u03b1 [TNF]) in the short, medium, and long term. Neonate male Wistar rats were randomized to receive a brain insult that could be either ischemic (left carotid artery ligation [LCAL]), hypoxic (8% oxygen chamber), hypoxic\u2013ischemic (LCAL and hypoxic chamber), sham\u2010ischemic, or sham\u2010hypoxic. Neuronal activity (<jats:italic>c\u2010Fos<\/jats:italic>activation at region CA1 and dentate gyrus of the hippocampus), nociceptive behavior (von Frey, tail\u2010flick, and hot\u2010plate tests), neuroplasticity mediators (BDNF, TNF), and a cellular injury marker (lactase dehydrogenase [LDH]) were assessed in blood serum 14, 30, and 60 days after birth. Neonatal HIE persistently reduced<jats:italic>c\u2010Fos<\/jats:italic>activation in the ipsilateral hippocampal region CA1; however, contralateral<jats:italic>c\u2010Fos<\/jats:italic>reduction appeared only 7 weeks after the event. Neonatal HIE acutely reduced the paw withdrawal threshold (von Frey test), but this returned to normal by the 30th postnatal day. Hypoxia reduced serum LDH levels. Serum neuroplasticity mediators increased with age, and neonatal HIE did not affect their ontogeny. Neonatal HIE\u2010induced reduction in neuronal activity occurs acutely in the ipsilateral hippocampal region CA1 and persists for at least 60 days, but the contralateral effect of the insult is delayed. Alterations in the nociceptive response are acute and self\u2010limited. Serum neuroplasticity mediators increase with age, and remain unaffected by HIE.<\/jats:p>","DOI":"10.1016\/j.ijdevneu.2014.09.003","type":"journal-article","created":{"date-parts":[[2014,9,27]],"date-time":"2014-09-27T19:49:15Z","timestamp":1411847355000},"page":"213-222","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Neonatal hypoxic\u2013ischemic encephalopathy reduces<i>c\u2010Fos<\/i>activation in the rat hippocampus: evidence of a long\u2010lasting effect"],"prefix":"10.1002","volume":"38","author":[{"given":"Andressa","family":"Souza","sequence":"first","affiliation":[{"name":"Graduate Program in Medicine: Medical Sciences Universidade Federal do Rio Grande do Sul 90035\u2010003 Porto Alegre Brazil"},{"name":"Pain Pharmacology and Animal Models of Neuromodulation Laboratory Department of Pharmacology Institute of Basic Health Sciences Universidade Federal do Rio Grande do Sul 90050\u2010170 Porto Alegre 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