In both control and trisomic mice, cortex showed the fewest sex differences: levels of only one protein differed in control mice, and 13 and 8 were altered in female and male Dp10, respectively.
Consistent with a role of MeCP2 in enhancing EGR2, Mecp2-deficient mouse cortex samples showed significantly reduced EGR2 by quantitative immunofluorescence.
Measurements across tangential sections show 18% shrinkage in the rostrocaudal axis (p = 0.006, one way ANOVA), but not in the mediolateral axis (p = 0.942, one way ANOVA, right ). (C ) TEM of cryo fixed (left ) and chemically fixed (right ) neuropil from the adult mouse cerebral cortex show reduction in the extracellular space (pseudo-coloured in blue) after chemical fixation.
Mouse retrosplenial granular cortex showing expression of laminin (A) and ZO1 (C) at lectin-labeled vasculature, with GFAP immunofluorescence; (B) Quantification of (A); (D) quantification of (C); **, P < 0.01, ***, P < 0.001, mean ± SEM; a.u. represents arbitrary unit.
Semi-quantitative analysis show that, relative to the β-synuclein levels in wild type mice, the ventral midbrain, but not cortex, shows increased levels of β-synuclein in α-synuclein null mice (Fig. 5B).
In both mouse and human GA1 encephalopathy, the cortex shows transient and more progressive degeneration while the striatum is injured more rapidly and completely [ 42].
Temporal analysis of miR-9 expression in mouse cortex by in situ hybridization (ISH) showed that the mature miR-9 was extensively expressed in the VZ/SVZ progenitors.
Unlike in wild-type mice, the reeler cortex showed no appreciable changes in MEMRI signal, consistent with absence of cortical laminae in histological slides.
More recently, oscillations in regulatory gene expression have been shown to take place in neural progenitors of the mouse cortex.
As shown in the figure, in this analysis the different parts of the mouse cortex are divided over different components.
