Pharmacology & Toxicology Poster Session

Re^2: Poster 719


On Mon Dec 7, hilaire wrote
>On Sun Dec 6, Grover wrote
>>Dr. Bou: Great presentation.  Hope you have fun at the meeting. You conclude that Tg8 mutant mice obtained from C3H mice by disrupting the gene encoding monoamine oxidase-A - the serotonin (5-HT) degradation enzyme - showed very high 5-HT levels at birth and that is how the respiration rate in these rats was abnormal.  How selective is monoamine oxidase A for serotonin?  I understood that it was not very selective and if so how uniquely can you interpret your results?
>Dr. Grove: Many thanks for your comments and question. I was trying to answer several times but I had some problems with this nice soft...
>My response: althought MAOA may be concerned with dopamine, 5-HT is a better substrate for MAOA. (Ref: Murphy,Substrate selective monoamine oxidases. Biochem. Pharmacol. 27 (1996) 1889-1893). HPLC tests in wild and MAOA-deficient mice revealed only minor (but significant) changes in relation with catecholamines levels in CNS mutant (see Cases et al.,). In addition, on going-experiments are revealing that via 5-HT agents applied to pregnant mice, it is possible to (more or less) convert the neonatal respiratory pattern (and motoneuron morphology)from the wild type to the mutant type and vice-versa. But this is another story and it is too early to talk about.

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