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MMP-9 knockout mice show behavioral impairments in hippocampus-dependent associative learning [13].
STOP (Stable Tubulin-Only Polypeptide) null mice show behavioral deficits, impaired synaptic plasticity, decrease in synaptic vesicular pools and disturbances in dopaminergic transmission, and are considered a neurodevelopmental model of schizophrenia.
These longer-lived Sirt6 mice show behavioral defects that are reminiscent of mouse models of Alzheimer or autism, for example.
As Hipk2 −/− mice show behavioral abnormalities consistent with cerebellar dysfunction, we investigated whether Hipk2 is involved in these neurological symptoms.
From existing animal models of PAK7, we do know that knockout mice are viable with no obvious developmental abnormalities but PAK6/PAK7 double knockout mice show behavioral and learning deficits suggesting functional redundancy between these isoforms (40).
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(2) KO mice showed behavioral abnormalities, namely hyperactivity and reduced anxiety-related behavior, both of which were supported by multiple different tests.
On the 28th day, 6-OHDA-injected mice showed behavioral impairments, a significant decrease in tyrosine hydroxylase (TH) and an increase in apoptosis.
It was demonstrated that the Tg2576 mice showed behavioral changes as early as 6 7 months of age [34].
In addition, these mice showed behavioral changes.
The MAOA-gene-knockout mice showed behavioral alteration [ 10].
An animal study, using DAOA transgenic mice, showed behavioral phenotypes associated with psychosis, some of which could be reversed with haloperidol [ 34].
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