The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib
The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, cultu...
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| Veröffentlicht in: | Molecular psychiatry 2010-12, Vol.15 (12), p.1140-1151 |
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| creator | Revest, J-M Kaouane, N. Mondin, M Le Roux, A. Rougé-Pont, F Vallée, M. Barik, J Tronche, F. Desmedt, A. Piazza, P |
| description | The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice (GR(NesCre)), we identified synapsin-Ia/Ib as one of the effectors of the glucocorticoid signaling cascade. Stress and glucocorticoid-induced activation of the GR modulate synapsin-Ia/Ib through two complementary mechanisms. First, glucocorticoids driving Egr-1 expression increase the expression of synapsin-Ia/Ib, and second, glucocorticoids driving MAPK activation increase its phosphorylation. Finally, we showed that blocking fucosylation of synapsin-Ia/Ib in the hippocampus inhibits its expression and prevents the glucocorticoid-mediated increase in stress-related memory. In conclusion, our data provide a complete molecular pathway (GR/Egr-1/MAPK/Syn-Ia/Ib) through which stress and glucocorticoids enhance the memory of stress-related events and highlight the function of synapsin-Ia/Ib as molecular effector of the behavioral effects of stress. |
| doi_str_mv | 10.1038/mp.2010.40 |
| format | Article |
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Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice (GR(NesCre)), we identified synapsin-Ia/Ib as one of the effectors of the glucocorticoid signaling cascade. Stress and glucocorticoid-induced activation of the GR modulate synapsin-Ia/Ib through two complementary mechanisms. First, glucocorticoids driving Egr-1 expression increase the expression of synapsin-Ia/Ib, and second, glucocorticoids driving MAPK activation increase its phosphorylation. Finally, we showed that blocking fucosylation of synapsin-Ia/Ib in the hippocampus inhibits its expression and prevents the glucocorticoid-mediated increase in stress-related memory. In conclusion, our data provide a complete molecular pathway (GR/Egr-1/MAPK/Syn-Ia/Ib) through which stress and glucocorticoids enhance the memory of stress-related events and highlight the function of synapsin-Ia/Ib as molecular effector of the behavioral effects of stress.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/mp.2010.40</identifier><identifier>PMID: 20368707</identifier><language>eng</language><publisher>Nature Publishing Group</publisher><subject>Analysis of Variance ; Animals ; Association Learning ; Avoidance Learning ; Corticosterone ; Early Growth Response Protein 1 ; Hippocampus ; Life Sciences ; Male ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Neurologic Mutants ; Mice, Transgenic ; Mitogen-Activated Protein Kinases ; Neurons ; PC12 Cells ; Rats ; Rats, Sprague-Dawley ; Receptors, Glucocorticoid ; Second Messenger Systems ; Signal Transduction ; Statistics, Nonparametric ; Stress, Psychological ; Synapsins</subject><ispartof>Molecular psychiatry, 2010-12, Vol.15 (12), p.1140-1151</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-7423-4158 ; 0000-0002-1179-7161 ; 0000-0001-7423-4158 ; 0000-0002-1179-7161</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://hal.science/hal-02325914$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Revest, J-M</creatorcontrib><creatorcontrib>Kaouane, N.</creatorcontrib><creatorcontrib>Mondin, M</creatorcontrib><creatorcontrib>Le Roux, A.</creatorcontrib><creatorcontrib>Rougé-Pont, F</creatorcontrib><creatorcontrib>Vallée, M.</creatorcontrib><creatorcontrib>Barik, J</creatorcontrib><creatorcontrib>Tronche, F.</creatorcontrib><creatorcontrib>Desmedt, A.</creatorcontrib><creatorcontrib>Piazza, P</creatorcontrib><title>The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib</title><title>Molecular psychiatry</title><description>The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice (GR(NesCre)), we identified synapsin-Ia/Ib as one of the effectors of the glucocorticoid signaling cascade. Stress and glucocorticoid-induced activation of the GR modulate synapsin-Ia/Ib through two complementary mechanisms. First, glucocorticoids driving Egr-1 expression increase the expression of synapsin-Ia/Ib, and second, glucocorticoids driving MAPK activation increase its phosphorylation. Finally, we showed that blocking fucosylation of synapsin-Ia/Ib in the hippocampus inhibits its expression and prevents the glucocorticoid-mediated increase in stress-related memory. In conclusion, our data provide a complete molecular pathway (GR/Egr-1/MAPK/Syn-Ia/Ib) through which stress and glucocorticoids enhance the memory of stress-related events and highlight the function of synapsin-Ia/Ib as molecular effector of the behavioral effects of stress.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Association Learning</subject><subject>Avoidance Learning</subject><subject>Corticosterone</subject><subject>Early Growth Response Protein 1</subject><subject>Hippocampus</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Memory</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Neurologic Mutants</subject><subject>Mice, Transgenic</subject><subject>Mitogen-Activated Protein Kinases</subject><subject>Neurons</subject><subject>PC12 Cells</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Glucocorticoid</subject><subject>Second Messenger Systems</subject><subject>Signal Transduction</subject><subject>Statistics, Nonparametric</subject><subject>Stress, Psychological</subject><subject>Synapsins</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqVistuwjAURC3UikfbTb_AWxaG69gmYYkqKpBYwjoyyaVxFduRb4qUv2-Q-gNdnZkzw9i7hJUEVax9t8pgLBombC51vhHG5MXTmJXZCi0LPWMLom-Ax2imbJaB2hQ55HN2OTfIMTQ2VOgx9DzeOPUJiUTC1vZYc48-poFfB_7V_lSxiql3VXQ18Ro7DCNj4DQE25EL4mjXx-sre77ZlvDtjy9s-bk_fxxEY9uyS87bNJTRuvKwO5UPB5nKzFbqu1T_-f4CwtxL7g</recordid><startdate>201012</startdate><enddate>201012</enddate><creator>Revest, J-M</creator><creator>Kaouane, N.</creator><creator>Mondin, M</creator><creator>Le Roux, A.</creator><creator>Rougé-Pont, F</creator><creator>Vallée, M.</creator><creator>Barik, J</creator><creator>Tronche, F.</creator><creator>Desmedt, A.</creator><creator>Piazza, P</creator><general>Nature Publishing Group</general><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-7423-4158</orcidid><orcidid>https://orcid.org/0000-0002-1179-7161</orcidid><orcidid>https://orcid.org/0000-0001-7423-4158</orcidid><orcidid>https://orcid.org/0000-0002-1179-7161</orcidid></search><sort><creationdate>201012</creationdate><title>The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib</title><author>Revest, J-M ; Kaouane, N. ; Mondin, M ; Le Roux, A. ; Rougé-Pont, F ; Vallée, M. ; Barik, J ; Tronche, F. ; Desmedt, A. ; Piazza, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-hal_primary_oai_HAL_hal_02325914v13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Association Learning</topic><topic>Avoidance Learning</topic><topic>Corticosterone</topic><topic>Early Growth Response Protein 1</topic><topic>Hippocampus</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Memory</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Neurologic Mutants</topic><topic>Mice, Transgenic</topic><topic>Mitogen-Activated Protein Kinases</topic><topic>Neurons</topic><topic>PC12 Cells</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Glucocorticoid</topic><topic>Second Messenger Systems</topic><topic>Signal Transduction</topic><topic>Statistics, Nonparametric</topic><topic>Stress, Psychological</topic><topic>Synapsins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Revest, J-M</creatorcontrib><creatorcontrib>Kaouane, N.</creatorcontrib><creatorcontrib>Mondin, M</creatorcontrib><creatorcontrib>Le Roux, A.</creatorcontrib><creatorcontrib>Rougé-Pont, F</creatorcontrib><creatorcontrib>Vallée, M.</creatorcontrib><creatorcontrib>Barik, J</creatorcontrib><creatorcontrib>Tronche, F.</creatorcontrib><creatorcontrib>Desmedt, A.</creatorcontrib><creatorcontrib>Piazza, P</creatorcontrib><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Revest, J-M</au><au>Kaouane, N.</au><au>Mondin, M</au><au>Le Roux, A.</au><au>Rougé-Pont, F</au><au>Vallée, M.</au><au>Barik, J</au><au>Tronche, F.</au><au>Desmedt, A.</au><au>Piazza, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib</atitle><jtitle>Molecular psychiatry</jtitle><date>2010-12</date><risdate>2010</risdate><volume>15</volume><issue>12</issue><spage>1140</spage><epage>1151</epage><pages>1140-1151</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice (GR(NesCre)), we identified synapsin-Ia/Ib as one of the effectors of the glucocorticoid signaling cascade. Stress and glucocorticoid-induced activation of the GR modulate synapsin-Ia/Ib through two complementary mechanisms. First, glucocorticoids driving Egr-1 expression increase the expression of synapsin-Ia/Ib, and second, glucocorticoids driving MAPK activation increase its phosphorylation. Finally, we showed that blocking fucosylation of synapsin-Ia/Ib in the hippocampus inhibits its expression and prevents the glucocorticoid-mediated increase in stress-related memory. In conclusion, our data provide a complete molecular pathway (GR/Egr-1/MAPK/Syn-Ia/Ib) through which stress and glucocorticoids enhance the memory of stress-related events and highlight the function of synapsin-Ia/Ib as molecular effector of the behavioral effects of stress.</abstract><pub>Nature Publishing Group</pub><pmid>20368707</pmid><doi>10.1038/mp.2010.40</doi><orcidid>https://orcid.org/0000-0001-7423-4158</orcidid><orcidid>https://orcid.org/0000-0002-1179-7161</orcidid><orcidid>https://orcid.org/0000-0001-7423-4158</orcidid><orcidid>https://orcid.org/0000-0002-1179-7161</orcidid></addata></record> |
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| subjects | Analysis of Variance Animals Association Learning Avoidance Learning Corticosterone Early Growth Response Protein 1 Hippocampus Life Sciences Male Memory Mice Mice, Inbred C57BL Mice, Knockout Mice, Neurologic Mutants Mice, Transgenic Mitogen-Activated Protein Kinases Neurons PC12 Cells Rats Rats, Sprague-Dawley Receptors, Glucocorticoid Second Messenger Systems Signal Transduction Statistics, Nonparametric Stress, Psychological Synapsins |
| title | The enhancement of stress-related memory by glucocorticoids depends on synapsin-Ia/Ib |
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