It seems that mice brains while less complex than ours are similar in circuitry -- so being called a mouse brain is no longer an insult -- therefore this was the closest they could get without human experimentation.
Control electron microscopy experiments using a GABAB2 knock out mouse brain revealed no labeling.
Moreover, in a study that focused on mtDNA mutations in mouse brain tumors, no pathogenic variants were detected across the mitochondrial genome in both induced and spontaneously developed tumors [ 49].
Moreover, transcriptome analysis in AICD transgenic mouse brain revealed no apparent difference between transgenic animals and littermate controls [ 20] and qPCR analysis of proposed target genes, including those studied here, failed to detect significant changes in mRNA expression.
Neuropathologic analyses of selected mouse brains found no spongiform encephalopathy or accumulations of PrP (data not shown).
Western blot analysis of isolated synaptic preparations from Rab18 −/−, and control, mouse brains showed no alterations in the levels of RAB3GAP1, RAB3GAP2 or RAB3A (supplementary material Fig. S1A C), suggesting that any neurological phenotype observed in Rab18 −/− mice was not a consequence of changes in these proteins.
Axial, coronal or sagittal sections from mutant mouse brains revealed no obstruction of intra- or extra-ventricular CSF flow, as seen by the presence of dye in the enlarged lateral ventricles, the third and fourth ventricles, the cisterns, and subarachnoid space.
While our results support the hypothesis of an altered PAF cycle in the Mecp2-null mouse brain, we have no direct evidence of changed PAF concentrations since PAF levels are below the detection threshold of our MRS experiments.
Monoclonal mouse anti-NeuN (used at 1 1,000) was raised against purified cell nuclei from mouse brain (Chemicon, code no. MAB377; Clone A60).
In the D-ribose-treated mouse brain, there seems no colocalization of the signal for either pS214 or pS396 phosphorylation staining of Tau and the AGE staining.
