<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet type="text/xsl" href="https://www.peertechzpublications.org/assets/xsl/oaitohtml.xsl"?>
<OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:mml="http://www.w3.org/1998/Math/MathML" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd">
										<responseDate>2026-04-14T09:54:01Z</responseDate>
										<request verb="GetRecord" metadataPrefix="oai_dc" identifier="oai:www.peertechzpublications.org:10.17352/2455-3484.000021">https://www.peertechzpublications.org/oai-pmh</request><GetRecord><record>
								<header>
									<identifier>oai:www.peertechzpublications.org:10.17352/2455-3484.000021</identifier>
									<datestamp>2017-05-12</datestamp>
									<setSpec>PTZ.JAMTS:VOL3</setSpec>
								</header>
								<metadata>
									<oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:mml="http://www.w3.org/1998/Math/MathML" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
										<dc:title>
										How the histamine N-methyltransferase inhibitor metoprine alleviates methamphetamine reward
										</dc:title><dc:creator>Nobue Kitanaka</dc:creator><dc:creator> Junichi Kitanaka</dc:creator><dc:creator> F Scott Hall</dc:creator><dc:creator> Satoshi Okumura#</dc:creator><dc:creator> Tomoyuki Sakamoto#</dc:creator><dc:creator> George R Uhl</dc:creator><dc:creator>Motohiko Takemura</dc:creator><dc:description>&lt;p&gt;Methamphetamine (METH) is a highly addictive psychomotor stimulant drug that is abused worldwide [1].&lt;br&gt;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,&lt;br&gt;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].&lt;br&gt;&lt;/p&gt;</dc:description>
										<dc:publisher>Journal of Addiction Medicine and Therapeutic Science - Peertechz Publications</dc:publisher>
										<dc:date>2017-05-12</dc:date>
										<dc:type>Review Article</dc:type>
										<dc:identifier>https://doi.org/10.17352/2455-3484.000021</dc:identifier>
										<dc:language>en</dc:language>
										<dc:rights>Copyright © Nobue Kitanaka et al.</dc:rights>
									</oai_dc:dc>
								</metadata>
							</record></GetRecord>
						</OAI-PMH>
