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Neonatal hypoxic-ischemic encephalopathy reduces c-Fos activation in the rat hippocampus: evidence of a long-lasting effect.
Int J Dev Neurosci
November 2014
Graduate Program in Medicine: Medical Sciences, Universidade Federal do Rio Grande do Sul, 90035-003, Porto Alegre, Brazil; Graduate Program in Biological Sciences: Physiology, Universidade Federal do Rio Grande do Sul, 90035-003, Porto Alegre, Brazil; Pain Pharmacology and Animal Models of Neuromodulation Laboratory, Department of Pharmacology, Institute of Basic Health Sciences, Universidade Federal do Rio Grande do Sul, 90050-170, Porto Alegre, Brazil; Animal Experimentation Unit, Hospital de Clínicas de Porto Alegre Graduate Research Group, 90035-003, Porto Alegre, Brazil. Electronic address:
The effect of neonatal hypoxic-ischemic encephalopathy (HIE) on maturation of nociceptive pathways has been sparsely explored. To investigate whether neonatal HIE alters neuronal activity, nociceptive behavior, and serum neuroplasticity mediators (brain-derived neurotrophic factor [BDNF] and tumor necrosis factor-α [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-ischemic (LCAL and hypoxic chamber), sham-ischemic, or sham-hypoxic.
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