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And yet, relatively few behavioral abnormalities have been reported in rpm-1 mutants.
However, similar behavioral abnormalities have been reported in Trpc2-/ mice, which have both VNO layers inactivated [ 2].
Progressive neuron loss, accompanied by neuroinflammation, can be found in cortical layers I/II [ 21], but early behavioral abnormalities have been reported well before the onset of neurodegeneration [ 22].
As similar behavioral abnormalities have been noted in rTg4510 mice (40), as well as other models of tauopathy (41– 46), the utilization of somatic brain transgenesis to deliver AAV1-TauP301L to neonatal mice recapitulates several key features characteristic of tauopathy but in the absence of overt neuronal loss.
First, a variety of neural and behavioral abnormalities have been described in individuals with TBS, including mental retardation, developmental delay, attention deficit hyperactivity disorder, hypoplasia of the corpus callosum, and seizures (Borozdin et al., 2006; Botzenhart et al., 2005; Cameron et al., 1991; Ishikiriyama et al., 1996).
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Although SynIII knockout (KO) mice display behavioral defects and changes in synaptic transmission, no gross brain abnormalities have been described (Feng et al., 2002; Porton et al., 2010).
Behavioral abnormalities have also been observed in patients with this deletion.
In the present study, we obtained no evidence of those pathological changes and mild behavioral abnormalities, which have been spatially and temporally linked to seismic experimentations and described in sperm whales from the Gulf of Mexico [46].
Behavioral abnormalities consistent with brain serotonergic damage have been reported in some polydrug users who also use the neurotoxin ecstasy (methylenedioxymethamphetamine, MDMA).
Genetically determined alterations in dopamine release and dopamine receptor expression in mice have been implicated in behavioral abnormalities induced by chronic stress [ 63].
Abnormalities in chromosome 20 have been linked to serious diseases, such as blood cancers.
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