Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors
Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overe...
Gespeichert in:
| Veröffentlicht in: | The Journal of neuroscience 1994-02, Vol.14 (2), p.763-773 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 773 |
|---|---|
| container_issue | 2 |
| container_start_page | 763 |
| container_title | The Journal of neuroscience |
| container_volume | 14 |
| creator | Tabb, JS Fanger, GR Wilson, EM Maue, RA Henderson, LP |
| description | Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overexpress the rat androgen receptor (AR) cDNA. Neither the expression nor function of ACh receptors was regulated by androgenic actions in these cells. However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influence posttranscriptional processing of Na channels in differentiating C2 cells. |
| doi_str_mv | 10.1523/jneurosci.14-02-00763.1994 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6576821</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>76349580</sourcerecordid><originalsourceid>FETCH-LOGICAL-c480t-b3e2168a738ba80137d122963caf88d8e839bfa9c64957ca1f1240b424a8090f3</originalsourceid><addsrcrecordid>eNpVkV9v0zAUxS0EGt3gIyBZCPaW4n9NbB6QUDVgaGISY8-W49itJ8fO7KRl3x6HVhU8-eH87rnn-gDwFqMlXhH64SGYKcWs3RKzCpEKoaamSywEewYWhRAVYQg_BwtEGlTVrGEvwXnOD6iACDdn4IxThGmNFmB3Nw1DMjm7GGC0MMfOTT3UWxWC8dBOQY-z5ALsnLUmmTA6NbqwgWsC-ylrb6A23meYR9X6Jxh3Bfp98CxUUiNUoUtxYwJMRpthjCm_Ai-s8tm8Pr4X4P7L1a_1t-rm9uv1-vNNpRlHY9VSQ3DNVUN5q3iJ3HSYEFFTrSznHTecitYqoWsmVo1W2OJyecsIK7RAll6ATwffYWp70-mSPikvh-R6lZ5kVE7-rwS3lZu4k_WqqTnBxeDyaJDi42TyKHuX53tVMHHKsnx8Wc1RAT8eQF2aycnY0xKM5Nya_P7j6v7n7d36WmImEZF_W5Nza2X4zb8xT6PHmor-7qirrJW3SQXt8gmjoua8FgV7f8C2brPdu2Rk7pX3xRTL_X5f1pI5MP0DkcyzPA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>76349580</pqid></control><display><type>article</type><title>Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Tabb, JS ; Fanger, GR ; Wilson, EM ; Maue, RA ; Henderson, LP</creator><creatorcontrib>Tabb, JS ; Fanger, GR ; Wilson, EM ; Maue, RA ; Henderson, LP</creatorcontrib><description>Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overexpress the rat androgen receptor (AR) cDNA. Neither the expression nor function of ACh receptors was regulated by androgenic actions in these cells. However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influence posttranscriptional processing of Na channels in differentiating C2 cells.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/jneurosci.14-02-00763.1994</identifier><identifier>PMID: 8301360</identifier><identifier>CODEN: JNRSDS</identifier><language>eng</language><publisher>Washington, DC: Soc Neuroscience</publisher><subject>Acetylcholine - pharmacology ; Androgen Antagonists - pharmacology ; Animals ; Biological and medical sciences ; Bungarotoxins - metabolism ; Cell Differentiation ; Cell Line ; Dihydrotestosterone - pharmacology ; Flutamide - analogs & derivatives ; Flutamide - pharmacology ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; Metribolone - metabolism ; Mice ; Muscles - cytology ; Muscles - metabolism ; Muscles - physiology ; Rats ; Receptors, Androgen - biosynthesis ; Receptors, Androgen - drug effects ; Receptors, Androgen - physiology ; Receptors, Cholinergic - biosynthesis ; Receptors, Cholinergic - drug effects ; Receptors, Cholinergic - metabolism ; Sodium Channels - drug effects ; Sodium Channels - physiology ; Striated muscle. Tendons ; Transfection ; Vertebrates: osteoarticular system, musculoskeletal system</subject><ispartof>The Journal of neuroscience, 1994-02, Vol.14 (2), p.763-773</ispartof><rights>1994 INIST-CNRS</rights><rights>1994 by Society for Neuroscience 1994</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-b3e2168a738ba80137d122963caf88d8e839bfa9c64957ca1f1240b424a8090f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6576821/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6576821/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3968869$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8301360$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tabb, JS</creatorcontrib><creatorcontrib>Fanger, GR</creatorcontrib><creatorcontrib>Wilson, EM</creatorcontrib><creatorcontrib>Maue, RA</creatorcontrib><creatorcontrib>Henderson, LP</creatorcontrib><title>Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overexpress the rat androgen receptor (AR) cDNA. Neither the expression nor function of ACh receptors was regulated by androgenic actions in these cells. However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influence posttranscriptional processing of Na channels in differentiating C2 cells.</description><subject>Acetylcholine - pharmacology</subject><subject>Androgen Antagonists - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bungarotoxins - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell Line</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>Flutamide - analogs & derivatives</subject><subject>Flutamide - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>Metribolone - metabolism</subject><subject>Mice</subject><subject>Muscles - cytology</subject><subject>Muscles - metabolism</subject><subject>Muscles - physiology</subject><subject>Rats</subject><subject>Receptors, Androgen - biosynthesis</subject><subject>Receptors, Androgen - drug effects</subject><subject>Receptors, Androgen - physiology</subject><subject>Receptors, Cholinergic - biosynthesis</subject><subject>Receptors, Cholinergic - drug effects</subject><subject>Receptors, Cholinergic - metabolism</subject><subject>Sodium Channels - drug effects</subject><subject>Sodium Channels - physiology</subject><subject>Striated muscle. Tendons</subject><subject>Transfection</subject><subject>Vertebrates: osteoarticular system, musculoskeletal system</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkV9v0zAUxS0EGt3gIyBZCPaW4n9NbB6QUDVgaGISY8-W49itJ8fO7KRl3x6HVhU8-eH87rnn-gDwFqMlXhH64SGYKcWs3RKzCpEKoaamSywEewYWhRAVYQg_BwtEGlTVrGEvwXnOD6iACDdn4IxThGmNFmB3Nw1DMjm7GGC0MMfOTT3UWxWC8dBOQY-z5ALsnLUmmTA6NbqwgWsC-ylrb6A23meYR9X6Jxh3Bfp98CxUUiNUoUtxYwJMRpthjCm_Ai-s8tm8Pr4X4P7L1a_1t-rm9uv1-vNNpRlHY9VSQ3DNVUN5q3iJ3HSYEFFTrSznHTecitYqoWsmVo1W2OJyecsIK7RAll6ATwffYWp70-mSPikvh-R6lZ5kVE7-rwS3lZu4k_WqqTnBxeDyaJDi42TyKHuX53tVMHHKsnx8Wc1RAT8eQF2aycnY0xKM5Nya_P7j6v7n7d36WmImEZF_W5Nza2X4zb8xT6PHmor-7qirrJW3SQXt8gmjoua8FgV7f8C2brPdu2Rk7pX3xRTL_X5f1pI5MP0DkcyzPA</recordid><startdate>19940201</startdate><enddate>19940201</enddate><creator>Tabb, JS</creator><creator>Fanger, GR</creator><creator>Wilson, EM</creator><creator>Maue, RA</creator><creator>Henderson, LP</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</general><scope>IQODW</scope><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><scope>5PM</scope></search><sort><creationdate>19940201</creationdate><title>Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors</title><author>Tabb, JS ; Fanger, GR ; Wilson, EM ; Maue, RA ; Henderson, LP</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-b3e2168a738ba80137d122963caf88d8e839bfa9c64957ca1f1240b424a8090f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Androgen Antagonists - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bungarotoxins - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell Line</topic><topic>Dihydrotestosterone - pharmacology</topic><topic>Flutamide - analogs & derivatives</topic><topic>Flutamide - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>Metribolone - metabolism</topic><topic>Mice</topic><topic>Muscles - cytology</topic><topic>Muscles - metabolism</topic><topic>Muscles - physiology</topic><topic>Rats</topic><topic>Receptors, Androgen - biosynthesis</topic><topic>Receptors, Androgen - drug effects</topic><topic>Receptors, Androgen - physiology</topic><topic>Receptors, Cholinergic - biosynthesis</topic><topic>Receptors, Cholinergic - drug effects</topic><topic>Receptors, Cholinergic - metabolism</topic><topic>Sodium Channels - drug effects</topic><topic>Sodium Channels - physiology</topic><topic>Striated muscle. Tendons</topic><topic>Transfection</topic><topic>Vertebrates: osteoarticular system, musculoskeletal system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tabb, JS</creatorcontrib><creatorcontrib>Fanger, GR</creatorcontrib><creatorcontrib>Wilson, EM</creatorcontrib><creatorcontrib>Maue, RA</creatorcontrib><creatorcontrib>Henderson, LP</creatorcontrib><collection>Pascal-Francis</collection><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tabb, JS</au><au>Fanger, GR</au><au>Wilson, EM</au><au>Maue, RA</au><au>Henderson, LP</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>1994-02-01</date><risdate>1994</risdate><volume>14</volume><issue>2</issue><spage>763</spage><epage>773</epage><pages>763-773</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><coden>JNRSDS</coden><abstract>Differentiation of skeletal muscle and the formation of the neuromuscular junction are regulated by steroid hormones. The effects of androgens on ion channel proteins central to neuromuscular signalling have been investigated in differentiating mouse muscle C2 cells and in C2 cells that stably overexpress the rat androgen receptor (AR) cDNA. Neither the expression nor function of ACh receptors was regulated by androgenic actions in these cells. However, voltage-dependent sodium (Na) current density was decreased by androgen treatment of C2 cells and was abolished, even in the absence of androgens, in C2 cells that overexpress the AR. The decrease in functional Na current was not accompanied by concomitant decreases in Na channel mRNA, suggesting that AR influence posttranscriptional processing of Na channels in differentiating C2 cells.</abstract><cop>Washington, DC</cop><pub>Soc Neuroscience</pub><pmid>8301360</pmid><doi>10.1523/jneurosci.14-02-00763.1994</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0270-6474 |
| ispartof | The Journal of neuroscience, 1994-02, Vol.14 (2), p.763-773 |
| issn | 0270-6474 1529-2401 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6576821 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Acetylcholine - pharmacology Androgen Antagonists - pharmacology Animals Biological and medical sciences Bungarotoxins - metabolism Cell Differentiation Cell Line Dihydrotestosterone - pharmacology Flutamide - analogs & derivatives Flutamide - pharmacology Fundamental and applied biological sciences. Psychology Gene Expression Metribolone - metabolism Mice Muscles - cytology Muscles - metabolism Muscles - physiology Rats Receptors, Androgen - biosynthesis Receptors, Androgen - drug effects Receptors, Androgen - physiology Receptors, Cholinergic - biosynthesis Receptors, Cholinergic - drug effects Receptors, Cholinergic - metabolism Sodium Channels - drug effects Sodium Channels - physiology Striated muscle. Tendons Transfection Vertebrates: osteoarticular system, musculoskeletal system |
| title | Suppression of sodium channel function in differentiating C2 muscle cells stably overexpressing rat androgen receptors |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T22%3A40%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Suppression%20of%20sodium%20channel%20function%20in%20differentiating%20C2%20muscle%20cells%20stably%20overexpressing%20rat%20androgen%20receptors&rft.jtitle=The%20Journal%20of%20neuroscience&rft.au=Tabb,%20JS&rft.date=1994-02-01&rft.volume=14&rft.issue=2&rft.spage=763&rft.epage=773&rft.pages=763-773&rft.issn=0270-6474&rft.eissn=1529-2401&rft.coden=JNRSDS&rft_id=info:doi/10.1523/jneurosci.14-02-00763.1994&rft_dat=%3Cproquest_pubme%3E76349580%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=76349580&rft_id=info:pmid/8301360&rfr_iscdi=true |