How the histamine N-methyltransferase inhibitor metoprine alleviates methamphetamine reward

Nobue Kitanaka, Junichi Kitanaka*, F Scott Hall, Satoshi Okumura#, Tomoyuki Sakamoto#, George R Uhl and Motohiko Takemura

Methamphetamine (METH) is a highly addictive psychomotor stimulant drug that is abused worldwide [1].
METH abuse results in numerous adverse effects after acute administration, as well as an array of adverse outcomes associated with binge use, long-term use, and withdrawal [2- 4]. Acutely METH releases dopamine from synaptic terminals through multiple actions that include inducing reverse transport of dopamine via the dopamine transporter (DAT), impairing the function of the vesicular monoamine transporter-2 (VMAT2), leading to increased cytoplasmic dopamine concentrations,
and inhibition of monoamine oxidase [5-8]. Moreover, these changes contribute to the production of oxidative metabolites, metabolic impairments, oxidative damage to dopamine terminals, and depletion of tissue dopamine levels [9-11]. METH and related drugs consequently produce broad effects on the central nervous system both acutely and chronically [12-14].

Keywords: Methamphetamine; Drug addiction; Reward; Histaminergic system; Metoprine; Histamine N-methyltransferase

Published on: May 12, 2017 Pages: 16-23

Full Text PDF Full Text HTML DOI: 10.17352/2455-3484.000021
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