Our data support the ‘continuous spatial coding’ hypothesis, indi

Our data support the ‘continuous spatial coding’ hypothesis, indicating

that, while based on the same fronto-parieto-occipital neural network than categorical spatial relations coding, the coding of coordinate spatial relations relies more heavily on attentional and executive processes, which could induce hemispheric differences similar to those described in the literature. The results also show that visuo-spatial working memory consists of a short-term posterior store with a capacity of up to three elements in the parietal and extrastriate cortices. This selleck chemicals store depends on the presence of a visible space categorization and thus can be used for the coding of categorical spatial relations. When no visible space categorization is given or when more than three elements have to be coded, additional attentional and executive processes are recruited, mainly located in the dorso-lateral prefrontal cortex. (C) 2007 Elsevier Ltd. All rights Silmitasertib purchase reserved.”

MHV-JHM strain of the murine coronavirus mouse hepatitis virus is much more neurovirulent than the MHV-A59 strain, although both strains use murine CEACAM1a (mCEACAM1a) as the receptor to infect murine cells. We previously showed that Ceacam1a(-/-) mice are completely resistant to MHV-A59 infection (E. Hemmila et al., J. Virol. 78:10156-10165, 2004). In vitro, MHV-JHM, but not MHV-A59, can spread from infected murine cells to cells that lack mCEACAM1a, a phenomenon called receptor-independent spread. To determine whether MHV-JHM could infect and spread in the brain independent of mCEACAM1a, we inoculated Ceacam1a(-/-) mice. Although Ceacam1a(-/-) mice TNF-alpha inhibitor were completely resistant to i.c. inoculation with 10(6) PFU of recombinant wild-type MHV-A59 (RA59) virus, these mice were killed by recombinant MHV-JHM (RJHM) and a chimeric virus containing the spike of MHV-JHM in the MHV-A59 genome (SJHM/RA59). Immunohistochemistry showed that RJHM and SJHM/RA59 infected all neural cell types and induced severe microgliosis in both

Ceacam1a(-/-) and wild-type mice. For RJHM, the 50% lethal dose (LD50) is < 10(1.3) in wild-type mice and 10(3.1) in Ceacam1a(-/-) mice. For SJHM/RA59, the LD50 is < 10(1.3) in wild-type mice and 10(3.6) in Ceacam1a(-/-) mice. This study shows that infection and spread of MHV-JHM in the brain are dependent upon the viral spike glycoprotein. RJHM can initiate infection in the brains of Ceacam1a(-/-) mice, but expression of mCEACAM1a increases susceptibility to infection. The spread of infection in the brain is mCEACAM1a independent. Thus, the ability of the MHV-JHM spike to mediate mCEACAM1a-independent spread in the brain is likely an important factor in the severe neurovirulence of MHV-JHM in wild-type mice.

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