| First Author | Xikota JC | Year | 2008 |
| Journal | Brain Res | Volume | 1241 |
| Pages | 148-56 | PubMed ID | 18840415 |
| Mgi Jnum | J:147621 | Mgi Id | MGI:3841550 |
| Doi | 10.1016/j.brainres.2008.08.097 | Citation | Xikota JC, et al. (2008) Mild cognitive deficits associated to neocortical microgyria in mice with genetic deletion of cellular prion protein. Brain Res 1241:148-56 |
| abstractText | The cellular prion protein (PrP(C)) has been implicated with the modulation of neuronal apoptosis, adhesion, neurite outgrowth and maintenance which are processes involved in the neocortical development. Malformations of cortical development (MCD) are frequently associated with neurological conditions including mental retardation, autism, and epilepsy. Here we investigated the behavioral performance of female adult PrP(C)-null mice (Prnp(0/0)) and their wild-type controls (Prnp(+/+)) presenting unilateral polymicrogyria, a MCD experimentally induced by neonatal freeze-lesion in the right hemisphere. Injured mice from both genotypes presented similar locomotor activity but Prnp(0/0) mice showed a tendency to increase anxiety-related responses when compared to Prnp(+/+) animals. Additionally, injured Prnp(0/0) mice have a poorer performance in the social recognition task than sham-operated and Prnp(+/+) injured ones. Moreover the step-down inhibitory avoidance task was not affected by the procedure or the genotype of the animals. These data suggest that the genetic deletion of PrP(C) confers increased susceptibility to short-term social memory deficits induced by neonatal freezing model of polymicrogyria in mice. |
