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MANGANESE-ENHANCED MRI (MEMRI) OF ONGOING INFLAMMATION AND DELAYED NEURONAL DEATH SIX WEEKS AFTER HYPOXIA-ISCHEMIA (HI) IN THE NEONATAL RAT BRAIN
  1. M Wideroe1,
  2. C Brekken2,
  3. A Kaavelars3,
  4. C Heijnen3,
  5. J Skranes1,
  6. A M Brubakk1
  1. 1Department of Paediatrics, NTNU, Trondheim, Norway
  2. 2Department of Circulation and Imaging, NTNU, Trondheim, Norway
  3. 3Laboratory of Psychoneuroimmunology, UMC, Utrecht, The Netherlands

Abstract

Objective To follow glial cell activation and delayed neuronal death in vivo using MEMRI.

Methods The RCA was ligated in 14 P7 Wistar pups followed by 8% O2 for 75 min. Eight HI pups were injected with MnCl2 (100 mM, 40 mg/kg) i.p. 8 hrs after HI, and 24 hrs prior to MRI at 6 wks. Six HI pups received NaCl. 3D T1-w MRI (7T) was performed 1 and 6 wks after HI. Pups were sacrificed at 6 wks. Coronal slices were stained with HE, MAP-2, ED-1, GFAP and Fluorojade B and compared with MRI.

Results ME areas at 1 week appeared cystic at 6 wks. At 6 wks, ED-1 positive cells (microglia), GFAP positive cells (astrocytes) and a few Fluorojade B cells (dying neurons) were seen on the brim of the remaining cortex, hippocampus and amygdale in most animals (Figure A,B,C), and correlated with ME on MRI in HI+Mn pups, but not in HI Controls. The clearest ME-area at 6 weeks was in thalamus and was related to calcification (Fig D).

Conclusion Inflammation can still be detected 6 wks after HI in the neonatal rat brain in vivo using MEMRI, but manganese also accumulates in calcifications.

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