Role of dopamine D1 receptor in 3-fluoromethamphetamine-induced neurotoxicity in mice
DC Field | Value | Language |
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dc.contributor.author | Phuong-Tram Nguyen | - |
dc.contributor.author | Shin, Eun-Joo | - |
dc.contributor.author | Dang, Duy-Khanh | - |
dc.contributor.author | Tran, Hai-Quyen | - |
dc.contributor.author | Jang, Choon-Gon | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Lee, Yu Jeung | - |
dc.contributor.author | Lee, Hyo Jong | - |
dc.contributor.author | Lee, Yong Sup | - |
dc.contributor.author | Yamada, Kiyofumi | - |
dc.contributor.author | Nabeshima, Toshitaka | - |
dc.contributor.author | Kim, Hyoung-Chun | - |
dc.date.available | 2019-01-22T14:13:30Z | - |
dc.date.issued | 2018-02 | - |
dc.identifier.issn | 0197-0186 | - |
dc.identifier.issn | 1872-9754 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1280 | - |
dc.description.abstract | 3-Fluoromethamphetamine (3-FMA) is an illegal designer drug of methamphetamine (MA) derivative. Up to date, little is known about the neurotoxic potential of 3-FMA. In the present study, we investigated the role of dopamine receptors in neurotoxicity induced by 3-FMA in comparison with MA (35 mg/kg, i.p.) as a control drug. Here we found that 3-FMA (40, 60 or 80 mg/kg, i.p.) produced mortality in a dose dependent manner in mice. Treatment with 3-FMA (40 mg/kg, i.p.) resulted in significant hyperthermia, oxidative stress and microgliosis (microglial differentiation into M1 phenotype) followed by proapoptotic changes and the induction of terminal deoxynucleotidyl transferase dUDP nick end labeling (TUNEL)-positive cells. Moreover, 3-FMA significantly produced dopaminergic impairments [i.e., increase in dopamine (DA) turnover rate and decreases in DA level, and in the expression of tyrosine hydroxylase (TH), dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT-2)] with behavioral impairments. These dopaminergic neurotoxic effects of 3-FMA were comparable to those of MA. SCH23390, a dopamine D1 receptor antagonist, but not sulpiride, a dopamine D2 receptor antagonist significantly attenuated 3-FMA-induced neurotoxicity. Although both SCH23390 and sulpiride attenuated MA-induced dopaminergic neurotoxicity, sulpiride is more effective than SCH23390 on the dopaminergic neurotoxicity. Interestingly, SCH23390 treatment positively modulated 3-FMA-induced microglial activation (i.e., SCH23390 inhibited M1 phenotype from 3-FMA insult, but activated M2 phenotype). Therefore, our results suggest that the activation of dopamine D1 receptor is critical to 3-FMA-induced neurotoxicity, while both dopamine D1 and D2 receptors (dopamine D2 receptor > dopamine D1 receptor) mediate MA-induced dopaminergic neurotoxicity. (C) 2017 Elsevier Ltd. All rights reserved. | - |
dc.format.extent | 16 | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.title | Role of dopamine D1 receptor in 3-fluoromethamphetamine-induced neurotoxicity in mice | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.neuint.2017.11.017 | - |
dc.identifier.bibliographicCitation | NEUROCHEMISTRY INTERNATIONAL, v.113, pp 69 - 84 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000428495900007 | - |
dc.identifier.scopusid | 2-s2.0-85036557418 | - |
dc.citation.endPage | 84 | - |
dc.citation.startPage | 69 | - |
dc.citation.title | NEUROCHEMISTRY INTERNATIONAL | - |
dc.citation.volume | 113 | - |
dc.type.docType | Article | - |
dc.publisher.location | 네델란드 | - |
dc.subject.keywordAuthor | 3-Fluoromethamphetamine | - |
dc.subject.keywordAuthor | Dopaminergic deficits | - |
dc.subject.keywordAuthor | Striatum | - |
dc.subject.keywordAuthor | Dopamine receptors | - |
dc.subject.keywordAuthor | Oxidative stress | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordPlus | METHAMPHETAMINE-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | DISMUTASE TRANSGENIC MICE | - |
dc.subject.keywordPlus | IN-SITU HYBRIDIZATION | - |
dc.subject.keywordPlus | KINASE C-DELTA | - |
dc.subject.keywordPlus | MICROGLIAL ACTIVATION | - |
dc.subject.keywordPlus | PARKINSONS-DISEASE | - |
dc.subject.keywordPlus | TYROSINE-HYDROXYLASE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | MOUSE-BRAIN | - |
dc.subject.keywordPlus | TRANSPORTER FUNCTION | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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