Inhibition of monoamine oxidase by d-methamphetamine
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Cited by (59)
Autophagy as a gateway for the effects of methamphetamine: From neurotransmitter release and synaptic plasticity to psychiatric and neurodegenerative disorders
2021, Progress in NeurobiologyCitation Excerpt :The former is present within catecholamine-containing neurons (DA, NE, and Epinephrine neurons), whereas the latter occurs mainly in 5-HT-containing and glial cells. Remarkably, METH inhibits MAO-A with a 10-fold higher affinity compared with MAO-B, which underlines the crucial role of MAO-A for METH-induced alterations of intracellular DA metabolism within DA terminals (Gesi et al., 2001; Suzuki et al., 1980). This may also include the uncoupling between MAO-A and aldehyde dehydrogenase (AD), thus occluding the AD-dependent conversion of the highly reactive by-product of DA oxidation 3,4-dihydroxyphenylacetaldehyde (DOPALD) into the quite inert 3,4-dihydroxyphenylacetic acid (DOPAC) (Agid et al., 1973; Gesi et al., 2001).
Effects of the GluN2B-selective antagonist Ro 63-1908 on acquisition and expression of methamphetamine conditioned place preference in male and female rats
2021, Drug and Alcohol DependenceCitation Excerpt :The results of this meta-analysis highlight the need to test novel molecular targets for the treatment of methamphetamine use disorder. Although methamphetamine’s primary mechanisms of action are to reverse the vesicular monoamine transporter (VMAT2) (Peter et al., 1994) and monoamine transporters, such as the dopamine transporter (DAT) (Eschleman et al., 1994), as well as to inhibit monoamine oxidase (MAO) (Suzuki et al., 1980), there is evidence that methamphetamine directly interacts with the glutamatergic system. Glutamate is the major excitatory neurotransmitter in the mammalian brain and binds to several types of metabotropic receptors (mGluRs) and ionotropic receptors (iGluRs), including N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (see Ozawa et al., 1998 for a review).
Neurologic complications of psychomotor stimulant abuse
2015, International Review of NeurobiologyCitation Excerpt :The drug then displaces the monoamine from the storage vesicles to the cytoplasm where they are reverse-transported out of the cell through the same transporters that pumped methamphetamine into the cell (Fleckenstein, Volz, Riddle, Gibb, & Hanson, 2007). Methamphetamine also decreases monoamine neurotransmitter reuptake and degradation (Suzuki, Hattori, Asano, Oya, & Katsumata, 1980). The net result is a rapid and sustained increase in the extracellular concentrations of monoamine neurotransmitters.
Neurologic Manifestations of Chronic Methamphetamine Abuse
2013, Psychiatric Clinics of North AmericaCitation Excerpt :This causes monamines to leave the vesicle and accumulate in the cytoplasm where they are reverse transported out of the cell through the same transporters that pumped methamphetamine into the cell.19,20 In addition to increasing their release, methamphetamine also decreases monoamine reuptake and enzyme degradation.21 The net result is that methamphetamine causes a rapid and sustained increase in the extracellular concentrations of monoamines.