Regional Differences in the Neuronal Expression of Cyclooxygenase-2 (COX-2) in the Newborn Pig Brain

  • Oláh Orsolya
    Department of Physiology, University of Szeged School of Medicine Department of Physiology, University of Szeged School of Medicine
  • Németh István
    Department of Dermatology and Allergology, University of Szeged School of Medicine Department of Dermatology and Allergology, University of Szeged School of Medicine
  • Tóth-Szuki Valéria
    Department of Physiology, University of Szeged School of Medicine Department of Physiology, University of Szeged School of Medicine
  • Bari Ferenc
    Department of Medical Physics and Informatics, University of Szeged School of Medicine Department of Medical Physics and Informatics, University of Szeged School of Medicine
  • Domoki Ferenc
    Department of Physiology, University of Szeged School of Medicine Department of Physiology, University of Szeged School of Medicine

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Cyclooxygenase (COX)-2 is the major constitutively expressed COX isoform in the newborn brain. COX-2 derived prostanoids and reactive oxygen species appear to play a major role in the mechanism of perinatal hypoxic-ischemic injury in the newborn piglet, an accepted animal model of the human term neonate. The study aimed to quantitatively determine COX-2 immunopositive neurons in different brain regions in piglets under normoxic conditions (n=15), and 4 hours after 10 min asphyxia (n=11). Asphyxia did not induce significant changes in neuronal COX-2 expression of any studied brain areas. In contrast, there was a marked regional difference in all experimental groups. Thus, significant difference was observed between fronto-parietal and temporo-occipital regions: 59±4% and 67±3% versus 41±2% and 31±3% respectively (mean±SEM, data are pooled from all subjects, n=26, p<0.05, vs. fronto-parietal region). In the hippocampus, COX-2 immunopositivity was rare (highest expression in CA1 region: 14±2%). The studied subcortical areas showed negligible COX-2 staining. Our findings suggest that asphyxia does not significantly alter the pattern of neuronal COX-2 expression in the early reventilation period. Furthermore, based on the striking differences observed in cortical neuronal COX-2 distribution, the contribution of COX-2 mediated neuronal injury after asphyxia may also show region-specific differences.<br>

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