The different roles of 5-HT1A/2A receptors in fluoxetine ameliorated pigmentation of C57BL/6 mouse skin in response to stress
Stress, specifically chronic unpredictable stress and chronic restrained stress, induce depigmentation in C57BL/6 mice. Fluoxetine promoted melanin production and the migration of melanocytes via 5-HT1A receptor and 5-HT2A receptor, respectively. [Display omitted] •Fluoxetine ameliorates CUMS and CR...
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| Veröffentlicht in: | Journal of dermatological science 2018-12, Vol.92 (3), p.222-229 |
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| creator | Zhou, Liangliang Cai, Minxuan Ren, Yingying Wu, Huali Liu, Meng Chen, Haijuan Shang, Jing |
| description | Stress, specifically chronic unpredictable stress and chronic restrained stress, induce depigmentation in C57BL/6 mice. Fluoxetine promoted melanin production and the migration of melanocytes via 5-HT1A receptor and 5-HT2A receptor, respectively.
[Display omitted]
•Fluoxetine ameliorates CUMS and CRS induced depigmentation in C57BL/6 mouse.•Fluoxetine induces melanogenesis via activating the phosphorylation of p38 MAPK signaling pathways.•5-HT1A and 2A receptors regulated fluoxetine increased melanocyte melanogenesis and migration.
5-HT1A receptor was participated in fluoxetine induced melanogenesis in melanocytes and in normal C57BL/6 mice, but we know little about whether other 5-HT receptors are involved in regulation of fluoxetine promotes pigmentation.
To investigate the role of 5-HT receptors in regulation of fluoxetine ameliorates chronic unpredictable mild stress (CUMS) and chronic restraint stress (CRS) induce hypopigmentation in C57BL/6 mice.
CUMS and CRS were used to induce depigmentation in mice and evaluate the effect of fluoxetine. Western blot, immunohistochemistry and Q-PCR assay were used to determine the levels of protein and mRNA. Masson Fontana staining was used for melanin staining and FITC-Phalloidin staining was used to detect the expression of F-actin. Zebrafish and B16F10 cells were used for the mechanism research.
Fluoxetine (2.6 mg/kg, ig) ameliorated hypopigmentation induced by CUMS and CRS in mice, significantly increased the mRNA and protein levels of 5-HT1 A and 5-HT2 A receptors in mice and B16F10 cells. The effect of fluoxetine on melanogenesis in B16F10 cells and zebrafish were inhibited by WAY100635 (a selective 5-HT1 A receptor antagonist) and ketanserin (a 5-HT2 A receptor antagonist), respectively. Activation of p38 MAPK signaling pathways was contributed to fluoxetine induced melanogenesis and inhibited by WAY100635, but not ketanserin. However, ketanserin selectively weakened the action of fluoxetine promoted migration and up-regulated Rab27a protein expression in B16F10 cells.
5-HT1 A and 2 A receptors contribute to melanogenesis and migration property of fluoxetine. The newly revealed mechanism indicates that fluoxetine and its analogues may be a potential drug for treatment of depigmentation disorders. |
| doi_str_mv | 10.1016/j.jdermsci.2018.10.002 |
| format | Article |
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[Display omitted]
•Fluoxetine ameliorates CUMS and CRS induced depigmentation in C57BL/6 mouse.•Fluoxetine induces melanogenesis via activating the phosphorylation of p38 MAPK signaling pathways.•5-HT1A and 2A receptors regulated fluoxetine increased melanocyte melanogenesis and migration.
5-HT1A receptor was participated in fluoxetine induced melanogenesis in melanocytes and in normal C57BL/6 mice, but we know little about whether other 5-HT receptors are involved in regulation of fluoxetine promotes pigmentation.
To investigate the role of 5-HT receptors in regulation of fluoxetine ameliorates chronic unpredictable mild stress (CUMS) and chronic restraint stress (CRS) induce hypopigmentation in C57BL/6 mice.
CUMS and CRS were used to induce depigmentation in mice and evaluate the effect of fluoxetine. Western blot, immunohistochemistry and Q-PCR assay were used to determine the levels of protein and mRNA. Masson Fontana staining was used for melanin staining and FITC-Phalloidin staining was used to detect the expression of F-actin. Zebrafish and B16F10 cells were used for the mechanism research.
Fluoxetine (2.6 mg/kg, ig) ameliorated hypopigmentation induced by CUMS and CRS in mice, significantly increased the mRNA and protein levels of 5-HT1 A and 5-HT2 A receptors in mice and B16F10 cells. The effect of fluoxetine on melanogenesis in B16F10 cells and zebrafish were inhibited by WAY100635 (a selective 5-HT1 A receptor antagonist) and ketanserin (a 5-HT2 A receptor antagonist), respectively. Activation of p38 MAPK signaling pathways was contributed to fluoxetine induced melanogenesis and inhibited by WAY100635, but not ketanserin. However, ketanserin selectively weakened the action of fluoxetine promoted migration and up-regulated Rab27a protein expression in B16F10 cells.
5-HT1 A and 2 A receptors contribute to melanogenesis and migration property of fluoxetine. The newly revealed mechanism indicates that fluoxetine and its analogues may be a potential drug for treatment of depigmentation disorders.</description><identifier>ISSN: 0923-1811</identifier><identifier>EISSN: 1873-569X</identifier><identifier>DOI: 10.1016/j.jdermsci.2018.10.002</identifier><identifier>PMID: 30527375</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>5-HT1A receptor ; 5-HT2A receptor ; Animals ; C57BL/6 mice ; Cell Line, Tumor ; Cell Movement - drug effects ; Disease Models, Animal ; Fluoxetine ; Fluoxetine - pharmacology ; Fluoxetine - therapeutic use ; Humans ; Male ; MAP Kinase Signaling System - drug effects ; Melanins - biosynthesis ; Melanocytes - drug effects ; Melanocytes - pathology ; Mice ; Mice, Inbred C57BL ; Pigmentation Disorders - drug therapy ; Pigmentation Disorders - etiology ; Pigmentation Disorders - pathology ; rab27 GTP-Binding Proteins - metabolism ; Receptor, Serotonin, 5-HT1A - metabolism ; Receptor, Serotonin, 5-HT2A - metabolism ; Serotonin - metabolism ; Serotonin Uptake Inhibitors - pharmacology ; Serotonin Uptake Inhibitors - therapeutic use ; Skin Pigmentation - drug effects ; Stress, Psychological - complications ; Up-Regulation - drug effects</subject><ispartof>Journal of dermatological science, 2018-12, Vol.92 (3), p.222-229</ispartof><rights>2018</rights><rights>Copyright © 2018. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-874ef9d753138ff123a26c70dcab92249d855ef6485adff784388708c9705ea43</citedby><cites>FETCH-LOGICAL-c392t-874ef9d753138ff123a26c70dcab92249d855ef6485adff784388708c9705ea43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jdermsci.2018.10.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30527375$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Liangliang</creatorcontrib><creatorcontrib>Cai, Minxuan</creatorcontrib><creatorcontrib>Ren, Yingying</creatorcontrib><creatorcontrib>Wu, Huali</creatorcontrib><creatorcontrib>Liu, Meng</creatorcontrib><creatorcontrib>Chen, Haijuan</creatorcontrib><creatorcontrib>Shang, Jing</creatorcontrib><title>The different roles of 5-HT1A/2A receptors in fluoxetine ameliorated pigmentation of C57BL/6 mouse skin in response to stress</title><title>Journal of dermatological science</title><addtitle>J Dermatol Sci</addtitle><description>Stress, specifically chronic unpredictable stress and chronic restrained stress, induce depigmentation in C57BL/6 mice. Fluoxetine promoted melanin production and the migration of melanocytes via 5-HT1A receptor and 5-HT2A receptor, respectively.
[Display omitted]
•Fluoxetine ameliorates CUMS and CRS induced depigmentation in C57BL/6 mouse.•Fluoxetine induces melanogenesis via activating the phosphorylation of p38 MAPK signaling pathways.•5-HT1A and 2A receptors regulated fluoxetine increased melanocyte melanogenesis and migration.
5-HT1A receptor was participated in fluoxetine induced melanogenesis in melanocytes and in normal C57BL/6 mice, but we know little about whether other 5-HT receptors are involved in regulation of fluoxetine promotes pigmentation.
To investigate the role of 5-HT receptors in regulation of fluoxetine ameliorates chronic unpredictable mild stress (CUMS) and chronic restraint stress (CRS) induce hypopigmentation in C57BL/6 mice.
CUMS and CRS were used to induce depigmentation in mice and evaluate the effect of fluoxetine. Western blot, immunohistochemistry and Q-PCR assay were used to determine the levels of protein and mRNA. Masson Fontana staining was used for melanin staining and FITC-Phalloidin staining was used to detect the expression of F-actin. Zebrafish and B16F10 cells were used for the mechanism research.
Fluoxetine (2.6 mg/kg, ig) ameliorated hypopigmentation induced by CUMS and CRS in mice, significantly increased the mRNA and protein levels of 5-HT1 A and 5-HT2 A receptors in mice and B16F10 cells. The effect of fluoxetine on melanogenesis in B16F10 cells and zebrafish were inhibited by WAY100635 (a selective 5-HT1 A receptor antagonist) and ketanserin (a 5-HT2 A receptor antagonist), respectively. Activation of p38 MAPK signaling pathways was contributed to fluoxetine induced melanogenesis and inhibited by WAY100635, but not ketanserin. However, ketanserin selectively weakened the action of fluoxetine promoted migration and up-regulated Rab27a protein expression in B16F10 cells.
5-HT1 A and 2 A receptors contribute to melanogenesis and migration property of fluoxetine. The newly revealed mechanism indicates that fluoxetine and its analogues may be a potential drug for treatment of depigmentation disorders.</description><subject>5-HT1A receptor</subject><subject>5-HT2A receptor</subject><subject>Animals</subject><subject>C57BL/6 mice</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Disease Models, Animal</subject><subject>Fluoxetine</subject><subject>Fluoxetine - pharmacology</subject><subject>Fluoxetine - therapeutic use</subject><subject>Humans</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Melanins - biosynthesis</subject><subject>Melanocytes - drug effects</subject><subject>Melanocytes - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pigmentation Disorders - drug therapy</subject><subject>Pigmentation Disorders - etiology</subject><subject>Pigmentation Disorders - pathology</subject><subject>rab27 GTP-Binding Proteins - metabolism</subject><subject>Receptor, Serotonin, 5-HT1A - metabolism</subject><subject>Receptor, Serotonin, 5-HT2A - metabolism</subject><subject>Serotonin - metabolism</subject><subject>Serotonin Uptake Inhibitors - pharmacology</subject><subject>Serotonin Uptake Inhibitors - therapeutic use</subject><subject>Skin Pigmentation - drug effects</subject><subject>Stress, Psychological - complications</subject><subject>Up-Regulation - drug effects</subject><issn>0923-1811</issn><issn>1873-569X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE9vGyEQxVGVqnHSfoWIYy9r82dZ2Fsdq40jWerFlXpDBIYWd3fZAq6SQ797sJz0WgkJ5um9GeaH0A0lS0potzosDw7SmG1YMkJVFZeEsDdoQZXkjej67xdoQXrGG6oovURXOR8IIYK1_Tt0yetDcikW6O_-J2AXvIcEU8EpDpBx9Fg02z1dr9gaJ7Awl5gyDhP2wzE-QgkTYDPCEGIyBRyew4-xxk0JcTqlN0Le7lYdHuMxA86_arKeBHmOUxVKxLnUKr9Hb70ZMnx4ua_Rty-f95tts_t6d79Z7xrLe1YaJVvwvZOCU668p4wb1llJnDUPPasrOSUE-K5VwjjvpWq5UpIo20siwLT8Gn08951T_H2EXPQYsoVhMBPUL2pGhaCiY0JWa3e22hRzTuD1nMJo0pOmRJ_Q64N-Ra9P6E96RV-DNy8zjg8juH-xV9bV8OlsgLrpnwBJ1xYwWXChMi7axfC_Gc-VE5g9</recordid><startdate>201812</startdate><enddate>201812</enddate><creator>Zhou, Liangliang</creator><creator>Cai, Minxuan</creator><creator>Ren, Yingying</creator><creator>Wu, Huali</creator><creator>Liu, Meng</creator><creator>Chen, Haijuan</creator><creator>Shang, Jing</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201812</creationdate><title>The different roles of 5-HT1A/2A receptors in fluoxetine ameliorated pigmentation of C57BL/6 mouse skin in response to stress</title><author>Zhou, Liangliang ; Cai, Minxuan ; Ren, Yingying ; Wu, Huali ; Liu, Meng ; Chen, Haijuan ; Shang, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-874ef9d753138ff123a26c70dcab92249d855ef6485adff784388708c9705ea43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>5-HT1A receptor</topic><topic>5-HT2A receptor</topic><topic>Animals</topic><topic>C57BL/6 mice</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Disease Models, Animal</topic><topic>Fluoxetine</topic><topic>Fluoxetine - pharmacology</topic><topic>Fluoxetine - therapeutic use</topic><topic>Humans</topic><topic>Male</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Melanins - biosynthesis</topic><topic>Melanocytes - drug effects</topic><topic>Melanocytes - pathology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Pigmentation Disorders - drug therapy</topic><topic>Pigmentation Disorders - etiology</topic><topic>Pigmentation Disorders - pathology</topic><topic>rab27 GTP-Binding Proteins - metabolism</topic><topic>Receptor, Serotonin, 5-HT1A - metabolism</topic><topic>Receptor, Serotonin, 5-HT2A - metabolism</topic><topic>Serotonin - metabolism</topic><topic>Serotonin Uptake Inhibitors - pharmacology</topic><topic>Serotonin Uptake Inhibitors - therapeutic use</topic><topic>Skin Pigmentation - drug effects</topic><topic>Stress, Psychological - complications</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Liangliang</creatorcontrib><creatorcontrib>Cai, Minxuan</creatorcontrib><creatorcontrib>Ren, Yingying</creatorcontrib><creatorcontrib>Wu, Huali</creatorcontrib><creatorcontrib>Liu, Meng</creatorcontrib><creatorcontrib>Chen, Haijuan</creatorcontrib><creatorcontrib>Shang, Jing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of dermatological science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Liangliang</au><au>Cai, Minxuan</au><au>Ren, Yingying</au><au>Wu, Huali</au><au>Liu, Meng</au><au>Chen, Haijuan</au><au>Shang, Jing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The different roles of 5-HT1A/2A receptors in fluoxetine ameliorated pigmentation of C57BL/6 mouse skin in response to stress</atitle><jtitle>Journal of dermatological science</jtitle><addtitle>J Dermatol Sci</addtitle><date>2018-12</date><risdate>2018</risdate><volume>92</volume><issue>3</issue><spage>222</spage><epage>229</epage><pages>222-229</pages><issn>0923-1811</issn><eissn>1873-569X</eissn><abstract>Stress, specifically chronic unpredictable stress and chronic restrained stress, induce depigmentation in C57BL/6 mice. Fluoxetine promoted melanin production and the migration of melanocytes via 5-HT1A receptor and 5-HT2A receptor, respectively.
[Display omitted]
•Fluoxetine ameliorates CUMS and CRS induced depigmentation in C57BL/6 mouse.•Fluoxetine induces melanogenesis via activating the phosphorylation of p38 MAPK signaling pathways.•5-HT1A and 2A receptors regulated fluoxetine increased melanocyte melanogenesis and migration.
5-HT1A receptor was participated in fluoxetine induced melanogenesis in melanocytes and in normal C57BL/6 mice, but we know little about whether other 5-HT receptors are involved in regulation of fluoxetine promotes pigmentation.
To investigate the role of 5-HT receptors in regulation of fluoxetine ameliorates chronic unpredictable mild stress (CUMS) and chronic restraint stress (CRS) induce hypopigmentation in C57BL/6 mice.
CUMS and CRS were used to induce depigmentation in mice and evaluate the effect of fluoxetine. Western blot, immunohistochemistry and Q-PCR assay were used to determine the levels of protein and mRNA. Masson Fontana staining was used for melanin staining and FITC-Phalloidin staining was used to detect the expression of F-actin. Zebrafish and B16F10 cells were used for the mechanism research.
Fluoxetine (2.6 mg/kg, ig) ameliorated hypopigmentation induced by CUMS and CRS in mice, significantly increased the mRNA and protein levels of 5-HT1 A and 5-HT2 A receptors in mice and B16F10 cells. The effect of fluoxetine on melanogenesis in B16F10 cells and zebrafish were inhibited by WAY100635 (a selective 5-HT1 A receptor antagonist) and ketanserin (a 5-HT2 A receptor antagonist), respectively. Activation of p38 MAPK signaling pathways was contributed to fluoxetine induced melanogenesis and inhibited by WAY100635, but not ketanserin. However, ketanserin selectively weakened the action of fluoxetine promoted migration and up-regulated Rab27a protein expression in B16F10 cells.
5-HT1 A and 2 A receptors contribute to melanogenesis and migration property of fluoxetine. The newly revealed mechanism indicates that fluoxetine and its analogues may be a potential drug for treatment of depigmentation disorders.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>30527375</pmid><doi>10.1016/j.jdermsci.2018.10.002</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of dermatological science, 2018-12, Vol.92 (3), p.222-229 |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | 5-HT1A receptor 5-HT2A receptor Animals C57BL/6 mice Cell Line, Tumor Cell Movement - drug effects Disease Models, Animal Fluoxetine Fluoxetine - pharmacology Fluoxetine - therapeutic use Humans Male MAP Kinase Signaling System - drug effects Melanins - biosynthesis Melanocytes - drug effects Melanocytes - pathology Mice Mice, Inbred C57BL Pigmentation Disorders - drug therapy Pigmentation Disorders - etiology Pigmentation Disorders - pathology rab27 GTP-Binding Proteins - metabolism Receptor, Serotonin, 5-HT1A - metabolism Receptor, Serotonin, 5-HT2A - metabolism Serotonin - metabolism Serotonin Uptake Inhibitors - pharmacology Serotonin Uptake Inhibitors - therapeutic use Skin Pigmentation - drug effects Stress, Psychological - complications Up-Regulation - drug effects |
| title | The different roles of 5-HT1A/2A receptors in fluoxetine ameliorated pigmentation of C57BL/6 mouse skin in response to stress |
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