Briefly, 1×104 susceptible N2aPK1 cells (gift from C. Weissmann) and resistant N2aR33 cells, maintained in opti-MEM (Gibco) plus 10% FBS, were exposed to a 10−5 dilution of strain RML PrPSc-infected murine brain homogenates for 48 hr in the presence or absence of 25, 50, 100 µM EIPA (Sigma).
We therefore analysed the developing murine brain and SNS for Gata-4 expression using immunohistochemistry.
In contrast, most cells derived from E11 murine brain stained positive for TUJ1 (Fig S9B of Supporting information, left panel).
The following lines of evidence argue in favour of this idea: first, coIP of endogenous proteins from murine brain was documented for dysbindin and pallidin (Nazarian et al., 2006) as well as for dysbindin and snapin (Talbot et al., 2006).
Moreover, individual mitochondria may display different bioenergetic-specific requirements for specific CLs as described for murine brain tissue.
Thresholds of detection are calculated for tracers with different distribution patterns in murine brain and in the heart, respectively, for the conditions of the multi-pinhole SPECT system employed.
For example, murine brain is altered in mice with one allele of Hdac1 without Hdac2 in neural cells, as opposed to neural cells with one allele of Hdac2 without Hdac130.
Jack et al. (2004) used a 9.4-T scanner and customized radiofrequency coil specific for imaging murine brain.
For example, during murine brain development, carnosine synthesis is only associated with the final stages of glial cell maturation [32].
The authors would like to thank Patty Ewing, D.V.M., M.S., DACVP, for reviewing the murine brain histopathology.
