Inhibition of monoamine oxidase by amphetamine and related compounds

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

“…A nine-fold difference was observed in the ICso of MDMA for MAO-A and MAO-B activity, show ing a selective potency of MDMA for MAO-A in rat brain homogenates (see Results, Figures 3 and 4, Table 2). This finding is consistent with studies showing the in vitro inhibition of MAO-A by amphetamine (Mantle et al 1976) and its analogue, PCA (Fuller et al 1965). A selective potency for the inhibition of the A subtype was also observed in vivo in rat brain homogenates 25 hours after the animals were injected with ampheta mine followed by phenelzine, a nonselective MAO in hibitor (Miller et al 1980).…”

“…Amphetamine has been reported as a competitive in hibitor of MAO-A activity (Mantle et al 1976) and a mixed inhibitor of MAO-B, that is, both the Vrnax and KM are changed (Pearce and Roth 1985). The results of this study show MDMA acts as a competitive inhibitor of MAO-A activity (see Results, Figure 1), whereas a mixed pattern of inhibition was observed for the MDMA inhibition of MAO-B (Figure 2).…”

Lobelane Inhibits Methamphetamine-Evoked Dopamine Release via Inhibition of the Vesicular Monoamine Transporter-2

“…Subsequently, available cytosolic DA is reversetransported by the DA transporter (DAT) into the extracellular space (Sulzer et al, 1995). In addition, methamphetamine inhibits monoamine oxidase (MAO), preventing DA metabolism into dihydroxyphenylacetic acid (DOPAC) and increasing cytosolic DA (Mantle et al, 1976). VMAT2 is an essential cellular component contributing to the increased extracellular DA concentrations and conditioned place preference (reward) induced by methamphetamine (Takahashi et al, 1997;Patel et al, 2003), which provides support for VMAT2 as a pharmacological target for the development of treatments for methamphetamine abuse.…”

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

“…Other Amphetamine Targets: Monoamine Oxidase, Tyrosine Hydroxylase, other Monoamine Transporters, Trace Amine-Associated Receptor 1, and Sigma Receptors. The ability of AMPH to block MAO has been repeatedly demonstrated both in vitro and in vivo (Mantle et al, 1976;Green and el Hait, 1978;Clarke et al, 1979;Miller et al, 1980;Robinson, 1985). AMPH also increases DA levels because of enhancement of TH function (Costa et al, 1972;Kuczenski, 1975), although high concentrations appear to decrease TH function (Kogan et al, 1976;Hotchkiss and Gibb, 1980).…”