To investigate whether En2−/− mice displayed abnormal behavior relevant to ASD, they were monitored in tasks designed to assess social maturation as well as learning and memory.
Thus, TSP-2-null mice display abnormal connective tissue architecture and increased angiogenesis in the dermis, and heal wounds at an accelerated rate.
Mutations in Drosophila Ago1 cause a severe loss of all types of neurons and glial cells while dicer deficient mice display abnormal neurogenesis and gliogenesis in the developing central nervous system (Kataoka et al., 2001; Kawase-Koga et al., 2009).
Behavioral analyses revealed paternally duplicated (patDp/+) mice displayed abnormal behaviors resembling the symptoms of ASDs.
RhoE deficient mice displayed abnormal motor patterns and motor behavior (Video S1).
Interestingly, Sei1-null mice displayed abnormal insulin secretion and blood glucose clearance, as well as a reduction in pancreatic β-cell surface.
Taken together, these results show that Pink1−/− mice display abnormal brain cytokine expression in response to peripheral LPS injection and suggest that Pink1−/− mice may be more susceptible to inflammation-induced DA neuron death [64], [65], [66], [67], [68].
We found that these mice display abnormal synapse organization and maturation in vitro, altered synapse density in the adult brain, enhanced glutamatergic transmission and reduced synaptic plasticity in CA1 hippocampus.
Conditional Smarca5-null mice display abnormal cerebellar foliation, ataxia-like symptoms and young mortality.
Furthermore, null Hmx2 mice display abnormal behaviours such as circling and hyperactivity.
