Abstract
In the mid-1950s the chance finding of iproniazid’s mood-elevating properties [1] led to the discovery that inhibition of monoamine oxidase (MAO) results in changes in cerebral function. Monoamine oxidase metabolizes and thus inactivates endogenous pressor amines (like serotonin and noradrenaline) as well as ingested amines absorbed from the gut (like tyramine). The therapeutic effect of MAOIs is supposed to be linked to an inhibition of the degradation of serotonin, noradrenaline and dopamine resulting in their increased availability. Among the various types of monoamine oxidases, those located in mitochondria, namely MAO-A and MAO-B, are of special interest for neuropsychiatry. Both enzymes are present in most tissues in the CNS but also in peripheral organs. MAO-A selectively deaminates serotonin and noradrenaline while benzylamines and phenythylamines are preferential substrates for MAO-B. In humans, dopamine is deaminated by both MAOs, hence the use of MAOIs in Parkinson’s disease. First generation MAOIs are non-selective (inhibiting both enzymes) and irreversible, meaning that MAO is permanently inhibited by their action. MAO activity only resumed after treatment had been discontinued for several weeks, allowing new enzyme to be generated.
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Buller, R., Karin, J.M. (2000). Monoamine oxidase inhibitors (including the newer reversible compounds). In: Briley, M., Nutt, D. (eds) Anxiolytics. Milestones in Drug Therapy. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8470-9_4
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DOI: https://doi.org/10.1007/978-3-0348-8470-9_4
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