Moore et al.
The
behavioral analyses of Moore et al are slightly unclear. While Moore et al
states what behaviors they are testing for they do not explain what these
behaviors exactly translate to in schizophrenia. I can only infer that the
“motor control in MAM-E17 and MAM-E15 offspring,” “prepulse inhibition of
startle,” and “orofacial dyskinesia” translate to various disorganized and
catatonic behaviors and “reversal learning” translates to perseveration or lack
thereof.
Otherwise,
the study was well designed and well established. The behavioral paradigms were
well explained in terms of method, as were their procedures. Most of their
findings were convincing in the sense that MAM-E15 was found not to be selective
of brain regions when MAM-17 was selective of subcortical and cerebral regions
more indicative of a schizophrenia-like pattern. This is displayed in Figure
4A, in which there was a change in cerebral cortical thickness demonstrating
significant differences in all three groups (control, MAM-E15 and MAM-E17). The
control rats demonstrate the most cerebral cortical thickness in Figure 4A
which highlights the prefrontal cortex, the frontoparietal cortex, the
perirhinal cortex and the occipital, followed by the MAM-E17 treated animals
and lastly, the MAM-E15 treated animals demonstrated the most reduced cerebral
cortical thickness, due to the fact that they had nonspecific reduction in
cortical areas.
Despite my
feelings of ambiguity on presentation of behavioral analyses and their
symptomatic counterparts, the authors' results were convincing in this domain as well.
Something that I found interesting was in reference to Figure 7A (ataxia score).
While MAM-E15 treated animals achieved a higher ataxia score than MAM-E17
treated animals with a 5.0mg/kg dose of PCP, they also had a significant
baseline score with no dose administered. This is also likely due to the fact that they experienced a nonspecific reduction in their cortical regions unlike
MAM-17 treated animals.
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