The effect of selective type A or type B monoamine oxidase inhibition on the intrasynaptosomal deamination of (3H)serotonin in rat spinal cord tissue.

The degree to which the type A and type B forms of monoamine oxidase participate in the intraneuronal deamination of (3H)serotonin (5-HT) was examined in synaptosomal-rich fractions of rat spinal cord tissue. Synaptosomes were labeled with (3H)5-HT and superfused with physiological buffers containing selective concentrations of a type A (clorgyline) or a type B (deprenyl) MAO inhibitor. The efflux of (3H)5-HT and newly-formed (3H)5-hydroxyindoleacetic acid (5-HIAA) was determined and compared to controls over time. In control samples, a slight decline in (3H)5-HT efflux occurred over the experimental superfusion period. However, a stable formation and efflux of (3H)5-HIAA was seen during this same period of time. When clorgyline was added to the superfusion buffer, a rapid decline in superfusate levels of (3H)5-HIAA was observed. Similar experiments in the presence of deprenyl were without effect. In order to elevate cytoplasmic concentrations of (3H)5-HT and therefore increase its chances for interaction with nerve terminal MAO, reserpine was added to the superfusion buffer. Reserpine caused a greater than 3-fold increase in (3H)5-HIAA formation with no change in (3H)5-HT efflux. Clorgyline inhibited this increase in (3H)5-HIAA formation but deprenyl was again without effect. In the presence of clorgyline, reserpine also caused an increase in (3H)5-HT efflux. These results strongly support the notion that 5-HT deamination within rat spinal cord nerve terminals occurs primarily, if not exclusively, through an interaction with type A MAO.