STEP signaling pathway mediates psychomotor stimulation and morphine withdrawal symptoms, but not for reward, analgesia and tolerance

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dc.contributor.authorYoon Jung kim-
dc.contributor.authorYoung Kang-
dc.contributor.authorHye-Yeon Park-
dc.contributor.authorJae-Ran Lee-
dc.contributor.authorDae Yeul Yu-
dc.contributor.authorT Murata-
dc.contributor.authorY Gondo-
dc.contributor.authorJung Hwan Hwang-
dc.contributor.authorYong-Hoon Kim-
dc.contributor.authorChul Ho Lee-
dc.contributor.authorM Rhee-
dc.contributor.authorP L Han-
dc.contributor.authorBong Hyun Chung-
dc.contributor.authorHyun-Jun Lee-
dc.contributor.authorKyoung Shim Kim-
dc.date.accessioned2017-04-19T10:18:10Z-
dc.date.available2017-04-19T10:18:10Z-
dc.date.issued2016-
dc.identifier.issnI0000028-
dc.identifier.uri10.1038/emm.2016.1.ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13152-
dc.description.abstractStriatal-enriched protein tyrosine phosphatase (STEP) is abundantly expressed in the striatum, which strongly expresses dopamine and opioid receptors and mediates the effects of many drugs of abuse. However, little is known about the role of STEP in opioid receptor function. In the present study, we generated STEP-targeted mice carrying a nonsense mutation (C230X) in the kinase interaction domain of STEP by screening the N-ethyl-N-nitrosourea (ENU)-driven mutant mouse genomic DNA library and subsequent in vitro fertilization. It was confirmed that the C230X nonsense mutation completely abolished functional STEP protein expression in the brain. STEP(C230X-/-) mice showed attenuated acute morphine-induced psychomotor activity and withdrawal symptoms, whereas morphine-induced analgesia, tolerance and reward behaviors were unaffected. STEP(C230X-/-) mice displayed reduced hyperlocomotion in response to intrastriatal injection of the μ-opioid receptor agonist DAMGO, but the behavioral responses to δ- and κ-opioid receptor agonists remained intact. These results suggest that STEP has a key role in the regulation of psychomotor action and physical dependency to morphine. These data suggest that STEP inhibition may be a critical target for the treatment of withdrawal symptoms associated with morphine.-
dc.publisherSpringer-Nature Pub Group-
dc.titleSTEP signaling pathway mediates psychomotor stimulation and morphine withdrawal symptoms, but not for reward, analgesia and tolerance-
dc.title.alternativeSTEP signaling pathway mediates psychomotor stimulation and morphine withdrawal symptoms, but not for reward, analgesia and tolerance-
dc.typeArticle-
dc.citation.titleExperimental and Molecular Medicine-
dc.citation.number0-
dc.citation.endPagee212-
dc.citation.startPagee212-
dc.citation.volume48-
dc.contributor.affiliatedAuthorJae-Ran Lee-
dc.contributor.affiliatedAuthorJung Hwan Hwang-
dc.contributor.affiliatedAuthorYong-Hoon Kim-
dc.contributor.affiliatedAuthorChul Ho Lee-
dc.contributor.affiliatedAuthorHyun-Jun Lee-
dc.contributor.affiliatedAuthorKyoung Shim Kim-
dc.contributor.alternativeName김윤정-
dc.contributor.alternativeName강영-
dc.contributor.alternativeName박혜연-
dc.contributor.alternativeName이재란-
dc.contributor.alternativeName유대열-
dc.contributor.alternativeNameMurata-
dc.contributor.alternativeNameGondo-
dc.contributor.alternativeName황정환-
dc.contributor.alternativeName김용훈-
dc.contributor.alternativeName이철호-
dc.contributor.alternativeName이명철-
dc.contributor.alternativeName한평림-
dc.contributor.alternativeName정봉현-
dc.contributor.alternativeName이현준-
dc.contributor.alternativeName김경심-
dc.identifier.bibliographicCitationExperimental and Molecular Medicine, vol. 48, pp. e212-e212-
dc.identifier.doi10.1038/emm.2016.1.-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
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