S Dos-Anjos

Publications (2)7.18 Total impact

• Source

  Available from: Sheyla Montori

  Article: AMPA receptor downregulation induced by ischaemia/reperfusion is attenuated by age and blocked by meloxicam

  S. Montori, S. Dos_Anjos, M. A. Ríos-Granja, C. C. Pérez-García, A. Fernández-López, B. Martínez-Villayandre
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  ABSTRACT: S. Montori, S. Dos_Anjos, M. A. Ríos-Granja, C. C. Pérez-García, A. Fernández-López and B. Martínez-Villayandre (2010) Neuropathology and Applied Neurobiology36, 436–447 AMPA receptor downregulation induced by ischaemia/reperfusion is attenuated by age and blocked by meloxicamAim: Stroke prevalence increases with age, while alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) and inflammation have been related to ischaemia-induced damage. This study shows how age and treatment with an anti-inflammatory agent (meloxicam) modify the levels of AMPAR subunits GluR1 and GluR2, as well as the mRNA levels of the GluR2-editing enzyme, ADAR2, in a global brain ischaemia/reperfusion (I/R) model. Methods: Two days after global ischaemia CA1, CA3, dentate gyrus and cerebral cortex were obtained from sham-operated and I/R-injured 3- and 18-month-old Sprague–Dawley rats. Real time polymerase chain reaction, Western blotting and immunohistochemical assays were performed. Meloxicam treatment was assayed on young animals. Results: Data showed that age attenuates the downregulation induced by I/R in the AMPAR subunits GluR1 and GluR2 and modifies the GluR1/GluR2 mRNA level ratio in a structure-dependent way. The study of the ADAR2 mRNA levels showed more downregulation in older animals than young ones. Meloxicam treatment prevented the transcriptional arrest induced by I/R. Conclusion: Our data suggest that changes in the AMPAR isoforms could be associated with ageing in the different structures studied. Although GluR2 editing seems to be involved in age-dependent vulnerability to ischaemia supporting the ‘GluR2 hypothesis’, this alone does not explain the differential vulnerability in the different brain regions. Finally, inflammation could play a role in protection from I/R-induced injury.
  Neuropathology and Applied Neurobiology 07/2010; 36(5):436 - 447. · 3.80 Impact Factor
• Source

  Available from: Arsenio Fernández-López

  Article: Early modifications in N-methyl-D-aspartate receptor subunit mRNA levels in an oxygen and glucose deprivation model using rat hippocampal brain slices.

  S Dos-Anjos, B Martínez-Villayandre, S Montori, C C Pérez-García, A Fernández-López
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  ABSTRACT: Glutamatergic N-methyl-d-aspartate NMDA receptors (NMDAR) are considered to play a key role in ischemia-induced damage. Long-term (hours) changes in their expression upon ischemia have been shown. Here we report short-term changes in the mRNA levels of the major hippocampal NMDAR subunits (NR1, NR2A and NR2B), as well as c-fos, in an ex vivo ischemia model using hippocampal slices. This effect can be observed also in a calcium free incubation solution. Striking early decreases in the NMDAR subunit mRNA levels were observed after 30 min of oxygen and glucose deprivation (OGD) as well as a partial recovery when the tissues were returned to the balanced salt solution (reperfusion-like period) for 3 h. Since OGD-induced damage has been reported to be a consequence of the increase in OGD-related glutamate release, we also analyzed NMDAR mRNA levels following increased glutamate levels in hippocampal sections in which no significant effects on NMDAR subunit mRNA levels were detected. Furthermore, we describe that the presence of MK-801 (a selective NMDAR antagonist), CNQX (a selective AMPA/kainate receptor antagonist) or their combined action in the incubation solution is able to induce a significant decrease in NMDAR expression but in these conditions the OGD does not induce further decreases in mRNA levels. We suggest that the mechanisms triggered during OGD to downregulate mRNA levels of NMDAR subunits could be the same than those induced by glutamate receptor antagonists.
  Neuroscience 09/2009; 164(3):1119-26. · 3.38 Impact Factor