Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons
Cerebellar granule neurons (CGNs) depend on potassium depolarization for survival and undergo apoptosis when deprived of depolarizing concentration of potassium. Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for th...
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| Veröffentlicht in: | Neuroscience letters 2006-10, Vol.407 (3), p.214-218 |
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| container_title | Neuroscience letters |
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| creator | Song, Bin Ma, Chi Gong, Shoufang Yuan, Zhongmin Li, Dan Liu, Wei Li, Wenming Chen, Ruzhu Zhu, Xiaonan Zeng, Jinsheng Han, Yifan Li, Mingtao |
| description | Cerebellar granule neurons (CGNs) depend on potassium depolarization for survival and undergo apoptosis when deprived of depolarizing concentration of potassium. Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for the activity-dependent survival in CGNs, but one recent study has revealed that ERK1/2 is activated by potassium deprivation and is required for apoptosis of CGNs. In this study we showed that ERK1/2 was inactivated, rather than activated, by potassium deprivation, indicating a lack of ERK1/2 involvement in potassium deprivation-induced apoptosis. Furthermore, suppression of potassium depolarization-induced activation of ERK1/2 with chemical inhibitor U0126 or PD98059 had no influence on the pro-survival effect of potassium depolarisation. Thus, ERK1/2 was not required for potassium depolarization-dependent survival of CGNs. Taken together, our findings suggest that ERK1/2 is not involved in activity-dependent survival or apoptosis of CGNs. |
| doi_str_mv | 10.1016/j.neulet.2006.08.040 |
| format | Article |
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Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for the activity-dependent survival in CGNs, but one recent study has revealed that ERK1/2 is activated by potassium deprivation and is required for apoptosis of CGNs. In this study we showed that ERK1/2 was inactivated, rather than activated, by potassium deprivation, indicating a lack of ERK1/2 involvement in potassium deprivation-induced apoptosis. Furthermore, suppression of potassium depolarization-induced activation of ERK1/2 with chemical inhibitor U0126 or PD98059 had no influence on the pro-survival effect of potassium depolarisation. Thus, ERK1/2 was not required for potassium depolarization-dependent survival of CGNs. Taken together, our findings suggest that ERK1/2 is not involved in activity-dependent survival or apoptosis of CGNs.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2006.08.040</identifier><identifier>PMID: 16973276</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Animals, Newborn ; Apoptosis ; Biological and medical sciences ; Cell Survival ; Cerebellar granule neurons ; Cerebellum - cytology ; Enzyme Activation ; ERK1/2 ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Extracellular Signal-Regulated MAP Kinases - physiology ; Fundamental and applied biological sciences. Psychology ; MAP Kinase Kinase Kinases - metabolism ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Neurons - enzymology ; Neurons - physiology ; Rats ; Rats, Sprague-Dawley ; Survival ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2006-10, Vol.407 (3), p.214-218</ispartof><rights>2006</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-a37838b07a2147b269d4d8d1a111acd3a14a42c71390462e2f3dad6b7e66d4053</citedby><cites>FETCH-LOGICAL-c390t-a37838b07a2147b269d4d8d1a111acd3a14a42c71390462e2f3dad6b7e66d4053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2006.08.040$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18171632$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16973276$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Song, Bin</creatorcontrib><creatorcontrib>Ma, Chi</creatorcontrib><creatorcontrib>Gong, Shoufang</creatorcontrib><creatorcontrib>Yuan, Zhongmin</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Li, Wenming</creatorcontrib><creatorcontrib>Chen, Ruzhu</creatorcontrib><creatorcontrib>Zhu, Xiaonan</creatorcontrib><creatorcontrib>Zeng, Jinsheng</creatorcontrib><creatorcontrib>Han, Yifan</creatorcontrib><creatorcontrib>Li, Mingtao</creatorcontrib><title>Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Cerebellar granule neurons (CGNs) depend on potassium depolarization for survival and undergo apoptosis when deprived of depolarizing concentration of potassium. Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for the activity-dependent survival in CGNs, but one recent study has revealed that ERK1/2 is activated by potassium deprivation and is required for apoptosis of CGNs. In this study we showed that ERK1/2 was inactivated, rather than activated, by potassium deprivation, indicating a lack of ERK1/2 involvement in potassium deprivation-induced apoptosis. Furthermore, suppression of potassium depolarization-induced activation of ERK1/2 with chemical inhibitor U0126 or PD98059 had no influence on the pro-survival effect of potassium depolarisation. Thus, ERK1/2 was not required for potassium depolarization-dependent survival of CGNs. Taken together, our findings suggest that ERK1/2 is not involved in activity-dependent survival or apoptosis of CGNs.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cell Survival</subject><subject>Cerebellar granule neurons</subject><subject>Cerebellum - cytology</subject><subject>Enzyme Activation</subject><subject>ERK1/2</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>MAP Kinase Kinase Kinases - metabolism</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Neurons - enzymology</subject><subject>Neurons - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Survival</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhhtR3NnVfyCSi966zdck6Ysgy-oKC170HKqTmiFjT7pN0s3u0X9uhhnYm6ci1FNVb56mecdoxyhTnw5dxGXE0nFKVUdNRyV90WyY0bzVveYvmw0VVLail_Squc75QCndsq183Vwx1WvBtdo0f-8eSwKH47iMkEgO-whjm3BfnwU9-R0iZMwEEpI4FRLiOo1rbYRIwJWwhvLUepwxeoyF5CWtYYWRTInAPM1lyiGfWIcJh3ql3tgniDU4qfHTFPOb5tUOxoxvL_Wm-fX17uftffvw49v32y8PrRM9LS0IbYQZqAbOpB646r30xjNgjIHzApgEyZ1mlZaKI98JD14NGpXykm7FTfPxvHdO058Fc7HHkE8fh4jTkq0yxvSylxWUZ9ClKeeEOzuncIT0ZBm1J_X2YM_q7Um9pcZW9XXs_WX_MhzRPw9dXFfgwwWA7GDcVQ0u5GfOMM2U4JX7fOaw2lgDJptdwOjQh4SuWD-F_yf5BywSpyg</recordid><startdate>20061030</startdate><enddate>20061030</enddate><creator>Song, Bin</creator><creator>Ma, Chi</creator><creator>Gong, Shoufang</creator><creator>Yuan, Zhongmin</creator><creator>Li, Dan</creator><creator>Liu, Wei</creator><creator>Li, Wenming</creator><creator>Chen, Ruzhu</creator><creator>Zhu, Xiaonan</creator><creator>Zeng, Jinsheng</creator><creator>Han, Yifan</creator><creator>Li, Mingtao</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</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></search><sort><creationdate>20061030</creationdate><title>Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons</title><author>Song, Bin ; Ma, Chi ; Gong, Shoufang ; Yuan, Zhongmin ; Li, Dan ; Liu, Wei ; Li, Wenming ; Chen, Ruzhu ; Zhu, Xiaonan ; Zeng, Jinsheng ; Han, Yifan ; Li, Mingtao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-a37838b07a2147b269d4d8d1a111acd3a14a42c71390462e2f3dad6b7e66d4053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cell Survival</topic><topic>Cerebellar granule neurons</topic><topic>Cerebellum - cytology</topic><topic>Enzyme Activation</topic><topic>ERK1/2</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>MAP Kinase Kinase Kinases - metabolism</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Neurons - enzymology</topic><topic>Neurons - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Survival</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Bin</creatorcontrib><creatorcontrib>Ma, Chi</creatorcontrib><creatorcontrib>Gong, Shoufang</creatorcontrib><creatorcontrib>Yuan, Zhongmin</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Li, Wenming</creatorcontrib><creatorcontrib>Chen, Ruzhu</creatorcontrib><creatorcontrib>Zhu, Xiaonan</creatorcontrib><creatorcontrib>Zeng, Jinsheng</creatorcontrib><creatorcontrib>Han, Yifan</creatorcontrib><creatorcontrib>Li, Mingtao</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><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Song, Bin</au><au>Ma, Chi</au><au>Gong, Shoufang</au><au>Yuan, Zhongmin</au><au>Li, Dan</au><au>Liu, Wei</au><au>Li, Wenming</au><au>Chen, Ruzhu</au><au>Zhu, Xiaonan</au><au>Zeng, Jinsheng</au><au>Han, Yifan</au><au>Li, Mingtao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2006-10-30</date><risdate>2006</risdate><volume>407</volume><issue>3</issue><spage>214</spage><epage>218</epage><pages>214-218</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Cerebellar granule neurons (CGNs) depend on potassium depolarization for survival and undergo apoptosis when deprived of depolarizing concentration of potassium. Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for the activity-dependent survival in CGNs, but one recent study has revealed that ERK1/2 is activated by potassium deprivation and is required for apoptosis of CGNs. In this study we showed that ERK1/2 was inactivated, rather than activated, by potassium deprivation, indicating a lack of ERK1/2 involvement in potassium deprivation-induced apoptosis. Furthermore, suppression of potassium depolarization-induced activation of ERK1/2 with chemical inhibitor U0126 or PD98059 had no influence on the pro-survival effect of potassium depolarisation. Thus, ERK1/2 was not required for potassium depolarization-dependent survival of CGNs. Taken together, our findings suggest that ERK1/2 is not involved in activity-dependent survival or apoptosis of CGNs.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16973276</pmid><doi>10.1016/j.neulet.2006.08.040</doi><tpages>5</tpages></addata></record> |
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| ispartof | Neuroscience letters, 2006-10, Vol.407 (3), p.214-218 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Animals, Newborn Apoptosis Biological and medical sciences Cell Survival Cerebellar granule neurons Cerebellum - cytology Enzyme Activation ERK1/2 Extracellular Signal-Regulated MAP Kinases - metabolism Extracellular Signal-Regulated MAP Kinases - physiology Fundamental and applied biological sciences. Psychology MAP Kinase Kinase Kinases - metabolism Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Neurons - enzymology Neurons - physiology Rats Rats, Sprague-Dawley Survival Vertebrates: nervous system and sense organs |
| title | Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons |
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