Analysis Tools
behavior/neurological
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• performance in the Morris water maze is similar for homozygous mutant and wild-type mice, suggesting the mutation does not affect spatial learning or spatial memory
• the time spent on the open arms of the elevated plus maze by homozygous mutant and wild-type mice is similar, indicating they experience similar anxiety levels
• in tests of sociability and social novelty, both homozygous and heterozygous mutant, like wild-type, mice spend more time in a chamber with an unfamiliar mouse than in an unoccupied chamber and more time in a chamber with a new unfamiliar mouse than with one to which they previously have been introduced
• homozygous mutant mice and wild-type mice consume similar amounts of a 10% sucrose solution relative to water consumed, consistent with normal reward responsiveness
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• both homozygous and heterozygous mutant mice exhibit disruption in latent inhibition (LI) of fear conditioning by pre-training exposure to the conditioned neutral stimulus (CS; sound) without the noxious unconditioned stimulus (US; shock)
• the antipsychotic clozapine corrects the LI disruption in homozygous mutant mice
• both homozygous and heterozygous mutant mice that are not not pre-exposed to the unpaired neutral stimulus acquire a strong US/CS association
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• homozygous mutant mice exhibit heightened horizontal locomotion in a novel open field throughout a 30-min trial; their vertical activity (rearing) is increased for the first 10 min
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• homozyous mutant mice require more training than do wild-type mice to achieve 70% correct choices on 3 consecutive days in a discrete paired-trial T-maze test with a 15 s choice delay
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• in a working memory test using a discrete paired-trial variable-delay T-maze task, homozygous mutant mice make fewer correct choices than do wild-type mice at shorter (5 s and 10 s) but not longer (30 s) choice delay intervals
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• in the absence of a prepulse, the amplitude of the acoustic startle response of homozygous mutant mice is significantly lower (p<0.01) than that of wild-type mice; this was found to be true over a wide range of startle intensities
• no correlation exists between the startle response and prepulse inhibition in homozygotes for this mutation (r = 0.16, p = 0.14)
• neither homozygous nor heterozygous mutants showed improvement in acoustic startle response when treated with haloperidol, clozapine, bupropion or rolipram
• the diminished startle response of mice with this mutation is not due to impaired hearing, as the auditory brainstem response (ABR) threshold of homozygous mutant mice at 16 kHz (40 +/- 2.6) is similar to that of wild
type mice (46 +/- 5.1)
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nervous system
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• magnetic resonance imaging (MRI) reveals that the brain volumes of mice homozygous or heterozygous for this mutation are 13% lower than those of wild-type mice
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• MRI reveals contraction of the thalamus in homozygous and heterozygous mutant mice
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• MRI reveals contraction of the entorhinal cortex in homozygous and heterozygous mutant mice
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• MRI reveals contraction around the cerebral cortex, without alteration of white-matter tracts, in homozygous and heterozygous mutant mice
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• MRI reveals contraction of the cerebella of homozygous and heterozygous mutant mice
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• mice homozygous for this mutation exhibit much lower prepulse inhibition (PPI; p<0.001), i.e., less reduction of the startle response following a prepulse, than do wild-type mice
• no correlation exists between the startle response and prepulse inhibition in homozygotes for this mutation (r = 0.16, p = 0.14)
• the typical antipsychotic haloperidol, a dopamine D2 receptor antagonist, partially normalizes the aberrant acoustic startle response and PPI of homozygous mutant mice
• the atypical antipsychotic clozapine, a combined dopamine D2 and serotonin receptor antagonist that also increases PPI in wild-type mice, partially normalizes the aberrant acoustic startle response and PPI of homozygous mutant mice
• the antidepressant bupropion, a combined dopamine and norepinephrine reuptake inhibitor, has no effect on the abnormal PPI of homozygous mutant mice
• the phosphodiesterase 4 (PDE4) inhibitor rolipram abolishes the PPI deficit of mice with this mutation
• the defective prepulse inhibition of mice with this mutation is not due to impaired hearing, as the auditory brainstem response (ABR) threshold of homozygous mutant mice at 16 kHz (40 +/- 2.6) is similar to that of wild-type mice (46 +/- 5.1)
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| schizophrenia | DOID:5419 |
OMIM:181500 |
J:120634 | |
