title: 11.7 T MR Imaging Revealed Dilatation of Virchow-Robin Spaces within Hippocampus in Maternally Lipopolysaccharide-exposed Rats.
abstract: OBJECTIVE
  11.7 Tesla MRI was examined to detect Virchow-Robin spaces (VRSs) smaller than 100 μm in the rat brain. The effects of maternal exposure to lipopolysaccharide (LPS) were evaluated on basis of the number of dilated VRSs in the offspring rat brain.
  
  
  METHODS
  T2-weighted MRI with an in-plane resolution up to 78 μm (repetition time = 5000 ms, echo time = 35 ms, slice thickness = 250 μm, imaging plane, coronal) was applied to identify VRSs. The dilated VRSs were counted in the rat brain at 5 and 10 weeks of age. The dams of half the number in each group were treated with LPS during pregnancy, and the remaining half was employed as control. LPS injection in gestation period was used to simulate maternal infections, the method of which was widely accepted as a rat model inducing neuropsychiatric disorders in the offspring. Effects of LPS exposure on the offspring rat brain were statistically investigated.
  
  
  RESULTS
  VRSs as small as 78 μm were successfully detected by the ultra high-field MRI. All dilated VRSs were observed within lacunosum molecular layer of hippocampus, and molecular and granular layers of dentate gyrus around hippocampal fissure. In juvenile rats (5 weeks of age), the number of dilated VRSs was significantly increased in the prenatal LPS exposed rat brain (12.9 ± 2.4, n = 7) than in the control (5.3 ± 1.5, n = 7, P < 0.05), while in young adult rats (10 weeks of age), there was no significant difference in the number between the prenatal LPS exposed rat brain (3.6 ± 0.9, n = 5) and the control (2.6 ± 0.4, n = 5).
  
  
  CONCLUSIONS
  The results of the present study suggested that maternal infection might cause dilatation of VRSs through neural damages especially in the dentate gyrus of the offspring rats. Thus, ultra high-field MRI can offer a promising diagnostic tool capable of determining the location of neonatal brain damage caused by maternal infections.
authors.affiliation: Division of Pathogenesis and Control of Oral Disease, Graduate School of Dentistry, Osaka University.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Ooi
authors.forename: Chizuko
authors.initials: C
authors.lastname: Inui-Yamamoto
authors.forename: Yoshichika
authors.initials: Y
authors.lastname: Yoshioka
authors.forename: Akitoshi
authors.initials: A
authors.lastname: Seiyama
authors.forename: Junji
authors.initials: J
authors.lastname: Seki
mesh_terms: D000818:Animals; D005260:Female; D006624:Hippocampus / Q000000981:diagnostic imaging* / Q000187:drug effects* / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000008:administration & dosage*; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000000981:diagnostic imaging*; D051381:Rats; D017208:Rats, Wistar; D013346:Subarachnoid Space / Q000473:pathology
chemical_list: D008070:Lipopolysaccharides