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The long\u2010term effects of meth within the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> include neuronal plasticity changes, blood\u2013brain barrier compromise, inflammation, electrical dysfunction, neuronal\/glial toxicity, and an increased risk to infectious diseases including <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>. Most of the reported meth effects in the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> are related to dysregulation of chemical synapses by altering the release and uptake of neurotransmitters, especially dopamine, norepinephrine, and epinephrine. However, little is known about the effects of meth on connexin (Cx) containing channels, such as gap junctions (<jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content>) and hemichannels (<jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content>). We examined the effects of meth on Cx expression, function, and its role in Neuro<jats:styled-content style=\"fixed-case\">AIDS<\/jats:styled-content>. We found that meth altered Cx expression and localization, decreased <jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content> communication between neurons and astrocytes, and induced the opening of Cx43\/Cx36 <jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content>. Furthermore, we found that these changes in <jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content> induced by meth treatment were mediated by activation of dopamine receptors, suggesting that dysregulation of dopamine signaling induced by meth is essential for <jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content> compromise. Meth\u2010induced changes in <jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content> contributed to amplified <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> toxicity by dysregulating glutamate metabolism and increasing the susceptibility of neurons and astrocytes to bystander apoptosis induced by <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>. Together, our results indicate that connexin containing channels, <jats:styled-content style=\"fixed-case\">GJ<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HC<\/jats:styled-content>, are essential in the pathogenesis of meth and increase the sensitivity of the <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> to <jats:styled-content style=\"fixed-case\">HIV CNS<\/jats:styled-content> disease.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13603-fig-0007-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>Methamphetamine (meth) is an extremely addictive central nervous system stimulant. Meth reduced gap junctional (GJ) communication by inducing internalization of connexin\u201043 (Cx43) in astrocytes and reducing expression of Cx36 in neurons by a mechanism involving activation of dopamine receptors (see cartoon). Meth\u2010induced changes in Cx containing channels increased extracellular levels of glutamate and resulted in higher sensitivity of neurons and astrocytes to apoptosis in response to HIV infection.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.13603","type":"journal-article","created":{"date-parts":[[2016,3,8]],"date-time":"2016-03-08T07:44:47Z","timestamp":1457423087000},"page":"561-575","source":"Crossref","is-referenced-by-count":44,"title":["Methamphetamine compromises gap junctional communication in astrocytes and neurons"],"prefix":"10.1111","volume":"137","author":[{"given":"Paul","family":"Castellano","sequence":"first","affiliation":[{"name":"Public Health Research Institute (PHRI) New Jersey Medical School Rutgers University Newark New Jersey USA"},{"name":"Department of Microbiology and Molecular Genetics New Jersey Medical School Rutgers University Newark New Jersey USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chisom","family":"Nwagbo","sequence":"additional","affiliation":[{"name":"Public Health Research Institute (PHRI) New Jersey Medical School Rutgers University Newark New Jersey USA"},{"name":"Department of Microbiology and Molecular Genetics New Jersey Medical School Rutgers University Newark New Jersey USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis R.","family":"Martinez","sequence":"additional","affiliation":[{"name":"New York Institute of Technology College of Osteopathic Medicine Old Westbury New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eliseo A.","family":"Eugenin","sequence":"additional","affiliation":[{"name":"Public Health Research Institute (PHRI) New Jersey Medical School Rutgers University Newark New Jersey USA"},{"name":"Department of Microbiology and Molecular Genetics New Jersey Medical School Rutgers University Newark New Jersey USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,4,18]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fncel.2014.00306"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11910-013-0387-7"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.6512-10.2011"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1080\/09540121.2014.985183"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.902650310"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/scdb.1998.0235"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-420118-7.00001-9"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11481-006-9018-2"},{"key":"e_1_2_8_10_1","first-page":"40","article-title":"Connexin43 in MDCK cells: regulation by a tumor\u2010promoting phorbol ester and Ca2+","volume":"57","author":"Berthoud V. 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