Our in vivo measurements of small intestinal permeability indicated that these mice demonstrate abnormal small intestinal permeability at 4 weeks of age, which is as early a time point as we can measure.
Previous studies performed on these mice have demonstrated abnormal Shh signaling and phenotypes consistent with both reduced and increased Shh signaling activity [ 19, 22, 23].
While glycemia was similar after overnight fasting (respectively for P-P, P-7, M-P and M-7 groups: 82.3±0.5, 79.6±4, 98.5±17.8 and 71.2±10.2 mg/dl), the MSG-treated mice demonstrated an abnormal glucose tolerance test (Figure 1C).
An exception was that during the first two postnatal weeks, all hyperoxic mice demonstrated an abnormal breathing pattern when placed under stress, e.g. when the bedding was being changed or when mice were being weighed, breathing heavily with a 'clicking' noise.
C58/J mice of both sexes demonstrated abnormal repetitive behaviors, displaying excessive jumping and back flipping in both social and non-social situations.
Histological and immunohistochemical analyses of the sural nerve using neuronal marker protein gene product 9.5 (PGP 9.5) demonstrated abnormal nerve fiber morphology in cisplatin-treated mice.
This was illustrated by previous electrophysiological findings that demonstrated abnormal GC excitability in the α-CaMKII hKO mice 15, and similar excitability from the present study in pilocarpine-treated mice.
Previously, we demonstrated abnormal Purkinje cell dendritic morphology in 3-week-old Mwk mice (8).
In addition, Lxn-overexpressing cell demonstrated abnormal mitotic spindle formation.
12 Existing cells demonstrated abnormal axon and dendrite growth.
