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Function of endogenous monoamine oxidase inhibitors (tribulin)

  • Conference paper
MAO — The Mother of all Amine Oxidases

Part of the book series: Journal of Neural Transmission. Supplement ((NEURAL SUPPL,volume 52))

Summary

Recent research on tribulin [low molecular weight endogenous inhibitory activity of monoamine oxidase (MAO)] has confirmed that its level is increased in both human urine and rat tissues by stress or anxiety, and by anxiogenic drugs. However tribulin is now known to contain several different molecules. The raised inhibitory activity in rat tissues is selective for MAO-A. There is a parallel decrease in MAO-A activity ex vivo, suggesting a possible functional effect. Increase in endogenous MAO I may competitively inhibit the binding of irreversible MAO I drugs, and may also help to mediate some mood altering effects of other drugs, or procedures such as ECT. In human urine both MAO-A I and MAO-B I have been found to be increased in mild stress. Similar findings have been made with human saliva. Selective inhibitors of MAO-A have been identified from human urine, and pig brain, but it is not yet clear to what extent they account for the MAO-A I activity increased in stress.

Isatin is an endogenous selective inhibitor of MAO-B (Ki ~3 μM). It has a distinct distribution in rat brain, with highest concentration in the hippocampus of 0.1 μg/g. Its level is increased by pentylene tetrazole, and isatin is itself anxiogenic in rodent models. Its administration also increases monoamine levels in the brain. It is a potent antagonist of the ANP receptor, and it may act to link the control of monoamine function and natriuresis.

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© 1998 Springer-Verlag Wien

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Glover, V. (1998). Function of endogenous monoamine oxidase inhibitors (tribulin). In: Finberg, J.P.M., Youdim, M.B.H., Riederer, P., Tipton, K.F. (eds) MAO — The Mother of all Amine Oxidases. Journal of Neural Transmission. Supplement, vol 52. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6499-0_31

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  • DOI: https://doi.org/10.1007/978-3-7091-6499-0_31

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-211-83037-6

  • Online ISBN: 978-3-7091-6499-0

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