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Effect of MAO A knockout on catecholamines in mouse brain regions: dopamine and norepinephrine in the cortex are unaffected by MAO A deficiency

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The effect of a lack of the gene encoding monoamine oxidase A (MAO A) in transgenic Tg8 mice on the levels of norepinephrine (NE), dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the midbrain, hypothalamus, hippocampus, striatum, amygdala, and frontal cortex was studied. It was shown that mice with a genetic MAO A knockout differed from those of the initial C3H/HeJ strain by a higher level of NE in all brain regions but the frontal cortex. The increased dopamine level in the striatum, a lower level of its metabolite DOPAC and decreased DOPAC/DA ratio in the midbrain, hypothalamus, hippocampus, and striatum of Tg8 mice was found. There were no changes in the DOPAC level or in the DOPAC/DA ratio in the frontal cortex and amygdala.

The substantial (2.4 to 4.8-fold) decrease in the level of DOPAC in the midbrain, hypothalamus, hippocampus, and striatum shows significant impairment of dopamine oxidative deamination in MAO A-knockout mice. At the same time, the lack of any changes in the dopamine level in most of brain regions studied indicates rather effective compensation of the deficit in DA metabolism in Tg8 mice and explains the lack of severe behavioral and pathological consequences in MAO A genetic deficiency. The data show that DA and NE metabolism in brain regions is differently affected by the MAO A deficiency, and that catecholamines in the mouse frontal cortex are unaffected by the lack of MAO A. The results suggest that in different brain regions the relative roles of MAO A, MAO B and COMT in metabolism of catecholamines are different.


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