Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors
To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the c...
Gespeichert in:
| Veröffentlicht in: | Archives of toxicology 2015-11, Vol.89 (11), p.1981-1991 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1991 |
|---|---|
| container_issue | 11 |
| container_start_page | 1981 |
| container_title | Archives of toxicology |
| container_volume | 89 |
| creator | Dong, Yang-Ting Wang, Ya Wei, Na Zhang, Qi-Fang Guan, Zhi-Zhong |
| description | To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the control group ( |
| doi_str_mv | 10.1007/s00204-014-1408-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1751216869</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1751216869</sourcerecordid><originalsourceid>FETCH-LOGICAL-c475t-5076e2402a400c4de0cf0819c31cf95013edc10003df1f8d64171519a09320b03</originalsourceid><addsrcrecordid>eNqNkctuFDEQRS1ERIbAB7BBltiwaVJlu19LFJ5SIjawbjnucsZRtz3YbsF8Cb-LOzMghBQpKy_q1ClXXcZeILxBgPY8AQhQFaCqUEFXiUdsg0qKClrZPWYbkAqqum3wlD1N6RYARdfLJ-xU1ApbqGHDfr0j64zL3Hk-kY7e-Ruu_chnmkPc82B51DnxHy5vudnG4J3hdlpCDMklbkKMNOlMRyJviY9kIulEI6efu0gpueDTKrrCO_OV5POSjI5udWlDeT-ZbZicJx7J0C6HmJ6xE6unRM-P7xn79uH914tP1eWXj58v3l5WRrV1rmpoGxIKhFYARo0ExkKHvZFobF8DShpNuRXI0aLtxqbsjTX2Gnop4BrkGXt98O5i-L5QysPskqFp0p7CkgZsaxTYdE3_AFTWPZTPrOir_9DbsERfFrmjsGvaXhYKD5Qpx0yR7LCLbtZxPyAMa8DDIeChBDysAQ-i9Lw8mpfrmca_HX8SLYA4AKmU_A3Ff0bfa_0NAVSwnA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1735186793</pqid></control><display><type>article</type><title>Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Dong, Yang-Ting ; Wang, Ya ; Wei, Na ; Zhang, Qi-Fang ; Guan, Zhi-Zhong</creator><creatorcontrib>Dong, Yang-Ting ; Wang, Ya ; Wei, Na ; Zhang, Qi-Fang ; Guan, Zhi-Zhong</creatorcontrib><description>To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the control group (<0.5 ppm fluoride in drinking water) and the fluoride group (50 ppm fluoride) for 10 months of treatment. The pups born from SD mothers with or without chronic fluorosis were selected at postnatal days 1, 7, 14, 21 and 28 for experiments (10 for each age). Spatial learning and memory were evaluated by Morris water maze test. The expressions of M1 and M3 mAChRs at the protein and mRNA levels were determined by Western blotting and real-time PCR, respectively. In addition, the contents of
·
OH, H
2
O
2
, O
2
·−
and malondialdehyde (MDA), and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in brains were quantitated by biochemical methods. Our results showed that as compared to controls, the abilities of learning and memory were declined in the adult rats and the offspring rats of postnatal day 28 in the fluoride groups; the expressions of both M1 and M3 mAChRs were significantly reduced at protein and mRNA levels; and the levels of
·
OH, H
2
O
2
, O
2
·−
and MDA were significantly increased, while the activities of SOD and GSH-Px decreased. Interestingly, the decreased protein levels of M1 and M3 mAChRs were significantly correlated with the deficits of learning and memory and high level of oxidative stress induced by chronic fluorosis. Our results suggest that the mechanism for the deficits in learning and memory of rats with chronic fluorosis may be associated with the decreased expressions of M1 and M3 in mAChRs, in which the changes in the receptors might be the result of the high level of oxidative stress occurring in the disease.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-014-1408-2</identifier><identifier>PMID: 25417050</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animal cognition ; Animal memory ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Chronic Disease ; Disease Models, Animal ; Environmental Health ; Female ; Fluoridation ; Fluorosis, Dental - complications ; Gene Expression Regulation ; Glutathione Peroxidase - metabolism ; Hydrogen Peroxide - metabolism ; Inorganic Compounds ; Male ; Malondialdehyde - metabolism ; Maze Learning ; Memory Disorders - etiology ; Occupational Medicine/Industrial Medicine ; Oxidative Stress ; Pharmacology/Toxicology ; Rats ; Rats, Sprague-Dawley ; Receptor, Muscarinic M1 - genetics ; Receptor, Muscarinic M3 - genetics ; RNA, Messenger - metabolism ; Rodents ; Superoxide Dismutase - metabolism ; Time Factors ; Toxicity</subject><ispartof>Archives of toxicology, 2015-11, Vol.89 (11), p.1981-1991</ispartof><rights>Springer-Verlag Berlin Heidelberg 2014</rights><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-5076e2402a400c4de0cf0819c31cf95013edc10003df1f8d64171519a09320b03</citedby><cites>FETCH-LOGICAL-c475t-5076e2402a400c4de0cf0819c31cf95013edc10003df1f8d64171519a09320b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-014-1408-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-014-1408-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25417050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, Yang-Ting</creatorcontrib><creatorcontrib>Wang, Ya</creatorcontrib><creatorcontrib>Wei, Na</creatorcontrib><creatorcontrib>Zhang, Qi-Fang</creatorcontrib><creatorcontrib>Guan, Zhi-Zhong</creatorcontrib><title>Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>Arch Toxicol</addtitle><description>To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the control group (<0.5 ppm fluoride in drinking water) and the fluoride group (50 ppm fluoride) for 10 months of treatment. The pups born from SD mothers with or without chronic fluorosis were selected at postnatal days 1, 7, 14, 21 and 28 for experiments (10 for each age). Spatial learning and memory were evaluated by Morris water maze test. The expressions of M1 and M3 mAChRs at the protein and mRNA levels were determined by Western blotting and real-time PCR, respectively. In addition, the contents of
·
OH, H
2
O
2
, O
2
·−
and malondialdehyde (MDA), and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in brains were quantitated by biochemical methods. Our results showed that as compared to controls, the abilities of learning and memory were declined in the adult rats and the offspring rats of postnatal day 28 in the fluoride groups; the expressions of both M1 and M3 mAChRs were significantly reduced at protein and mRNA levels; and the levels of
·
OH, H
2
O
2
, O
2
·−
and MDA were significantly increased, while the activities of SOD and GSH-Px decreased. Interestingly, the decreased protein levels of M1 and M3 mAChRs were significantly correlated with the deficits of learning and memory and high level of oxidative stress induced by chronic fluorosis. Our results suggest that the mechanism for the deficits in learning and memory of rats with chronic fluorosis may be associated with the decreased expressions of M1 and M3 in mAChRs, in which the changes in the receptors might be the result of the high level of oxidative stress occurring in the disease.</description><subject>Animal cognition</subject><subject>Animal memory</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Environmental Health</subject><subject>Female</subject><subject>Fluoridation</subject><subject>Fluorosis, Dental - complications</subject><subject>Gene Expression Regulation</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Inorganic Compounds</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Maze Learning</subject><subject>Memory Disorders - etiology</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>Oxidative Stress</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Muscarinic M1 - genetics</subject><subject>Receptor, Muscarinic M3 - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Time Factors</subject><subject>Toxicity</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkctuFDEQRS1ERIbAB7BBltiwaVJlu19LFJ5SIjawbjnucsZRtz3YbsF8Cb-LOzMghBQpKy_q1ClXXcZeILxBgPY8AQhQFaCqUEFXiUdsg0qKClrZPWYbkAqqum3wlD1N6RYARdfLJ-xU1ApbqGHDfr0j64zL3Hk-kY7e-Ruu_chnmkPc82B51DnxHy5vudnG4J3hdlpCDMklbkKMNOlMRyJviY9kIulEI6efu0gpueDTKrrCO_OV5POSjI5udWlDeT-ZbZicJx7J0C6HmJ6xE6unRM-P7xn79uH914tP1eWXj58v3l5WRrV1rmpoGxIKhFYARo0ExkKHvZFobF8DShpNuRXI0aLtxqbsjTX2Gnop4BrkGXt98O5i-L5QysPskqFp0p7CkgZsaxTYdE3_AFTWPZTPrOir_9DbsERfFrmjsGvaXhYKD5Qpx0yR7LCLbtZxPyAMa8DDIeChBDysAQ-i9Lw8mpfrmca_HX8SLYA4AKmU_A3Ff0bfa_0NAVSwnA</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Dong, Yang-Ting</creator><creator>Wang, Ya</creator><creator>Wei, Na</creator><creator>Zhang, Qi-Fang</creator><creator>Guan, Zhi-Zhong</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature 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>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20151101</creationdate><title>Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors</title><author>Dong, Yang-Ting ; Wang, Ya ; Wei, Na ; Zhang, Qi-Fang ; Guan, Zhi-Zhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-5076e2402a400c4de0cf0819c31cf95013edc10003df1f8d64171519a09320b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animal cognition</topic><topic>Animal memory</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Environmental Health</topic><topic>Female</topic><topic>Fluoridation</topic><topic>Fluorosis, Dental - complications</topic><topic>Gene Expression Regulation</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Inorganic Compounds</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Maze Learning</topic><topic>Memory Disorders - etiology</topic><topic>Occupational Medicine/Industrial Medicine</topic><topic>Oxidative Stress</topic><topic>Pharmacology/Toxicology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Muscarinic M1 - genetics</topic><topic>Receptor, Muscarinic M3 - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Time Factors</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Yang-Ting</creatorcontrib><creatorcontrib>Wang, Ya</creatorcontrib><creatorcontrib>Wei, Na</creatorcontrib><creatorcontrib>Zhang, Qi-Fang</creatorcontrib><creatorcontrib>Guan, Zhi-Zhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dong, Yang-Ting</au><au>Wang, Ya</au><au>Wei, Na</au><au>Zhang, Qi-Fang</au><au>Guan, Zhi-Zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors</atitle><jtitle>Archives of toxicology</jtitle><stitle>Arch Toxicol</stitle><addtitle>Arch Toxicol</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>89</volume><issue>11</issue><spage>1981</spage><epage>1991</epage><pages>1981-1991</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><abstract>To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the control group (<0.5 ppm fluoride in drinking water) and the fluoride group (50 ppm fluoride) for 10 months of treatment. The pups born from SD mothers with or without chronic fluorosis were selected at postnatal days 1, 7, 14, 21 and 28 for experiments (10 for each age). Spatial learning and memory were evaluated by Morris water maze test. The expressions of M1 and M3 mAChRs at the protein and mRNA levels were determined by Western blotting and real-time PCR, respectively. In addition, the contents of
·
OH, H
2
O
2
, O
2
·−
and malondialdehyde (MDA), and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in brains were quantitated by biochemical methods. Our results showed that as compared to controls, the abilities of learning and memory were declined in the adult rats and the offspring rats of postnatal day 28 in the fluoride groups; the expressions of both M1 and M3 mAChRs were significantly reduced at protein and mRNA levels; and the levels of
·
OH, H
2
O
2
, O
2
·−
and MDA were significantly increased, while the activities of SOD and GSH-Px decreased. Interestingly, the decreased protein levels of M1 and M3 mAChRs were significantly correlated with the deficits of learning and memory and high level of oxidative stress induced by chronic fluorosis. Our results suggest that the mechanism for the deficits in learning and memory of rats with chronic fluorosis may be associated with the decreased expressions of M1 and M3 in mAChRs, in which the changes in the receptors might be the result of the high level of oxidative stress occurring in the disease.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25417050</pmid><doi>10.1007/s00204-014-1408-2</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0340-5761 |
| ispartof | Archives of toxicology, 2015-11, Vol.89 (11), p.1981-1991 |
| issn | 0340-5761 1432-0738 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1751216869 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Animal cognition Animal memory Animals Biomedical and Life Sciences Biomedicine Chronic Disease Disease Models, Animal Environmental Health Female Fluoridation Fluorosis, Dental - complications Gene Expression Regulation Glutathione Peroxidase - metabolism Hydrogen Peroxide - metabolism Inorganic Compounds Male Malondialdehyde - metabolism Maze Learning Memory Disorders - etiology Occupational Medicine/Industrial Medicine Oxidative Stress Pharmacology/Toxicology Rats Rats, Sprague-Dawley Receptor, Muscarinic M1 - genetics Receptor, Muscarinic M3 - genetics RNA, Messenger - metabolism Rodents Superoxide Dismutase - metabolism Time Factors Toxicity |
| title | Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T13%3A34%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Deficit%20in%20learning%20and%20memory%20of%20rats%20with%20chronic%20fluorosis%20correlates%20with%20the%20decreased%20expressions%20of%20M1%20and%20M3%20muscarinic%20acetylcholine%20receptors&rft.jtitle=Archives%20of%20toxicology&rft.au=Dong,%20Yang-Ting&rft.date=2015-11-01&rft.volume=89&rft.issue=11&rft.spage=1981&rft.epage=1991&rft.pages=1981-1991&rft.issn=0340-5761&rft.eissn=1432-0738&rft_id=info:doi/10.1007/s00204-014-1408-2&rft_dat=%3Cproquest_cross%3E1751216869%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1735186793&rft_id=info:pmid/25417050&rfr_iscdi=true |