Predicting and treating stress-Induced vulnerability to epilepsy and depression
Accumulation of stressful events can render individuals susceptible to develop epilepsy and comorbidities. Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold fo...
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Veröffentlicht in: | Annals of neurology 2015-07, Vol.78 (1), p.128-136 |
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container_title | Annals of neurology |
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creator | Becker, Christel Bouvier, Elodie Ghestem, Antoine Siyoucef, Safia Claverie, Damien Camus, Françoise Bartolomei, Fabrice Benoliel, Jean-Jacques Bernard, Christophe |
description | Accumulation of stressful events can render individuals susceptible to develop epilepsy and comorbidities. Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depression‐like profile and cognitive deficits. Low serum brain‐derived neurotrophic factor (BDNF) levels measured before SE identified this vulnerable population. Treatment with a BDNF analog before SE prevented the occurrence of comorbidities. Thus, vulnerability to comorbidities after epilepsy onset due to unresolved past stressful events may be predicted and reversed. Ann Neurol 2015;78:128–136 |
doi_str_mv | 10.1002/ana.24414 |
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Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depression‐like profile and cognitive deficits. Low serum brain‐derived neurotrophic factor (BDNF) levels measured before SE identified this vulnerable population. Treatment with a BDNF analog before SE prevented the occurrence of comorbidities. Thus, vulnerability to comorbidities after epilepsy onset due to unresolved past stressful events may be predicted and reversed. 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Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depression‐like profile and cognitive deficits. Low serum brain‐derived neurotrophic factor (BDNF) levels measured before SE identified this vulnerable population. Treatment with a BDNF analog before SE prevented the occurrence of comorbidities. Thus, vulnerability to comorbidities after epilepsy onset due to unresolved past stressful events may be predicted and reversed. Ann Neurol 2015;78:128–136</description><subject>Allostasis</subject><subject>Animals</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - drug effects</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Cognition Disorders - metabolism</subject><subject>Cognition Disorders - psychology</subject><subject>Depression - metabolism</subject><subject>Depression - psychology</subject><subject>Disease Models, Animal</subject><subject>Epilepsy</subject><subject>Epilepsy - chemically induced</subject><subject>Epilepsy - metabolism</subject><subject>Epilepsy - psychology</subject><subject>Excitatory Amino Acid Agonists - toxicity</subject><subject>Flavones - pharmacology</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Kainic Acid - toxicity</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Neurons and Cognition</subject><subject>Pituitary-Adrenal System - drug effects</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Social Environment</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - metabolism</subject><subject>Stress, Psychological - metabolism</subject><subject>Stress, Psychological - psychology</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EokvhwBdAkbiUQ1pPbMf2cVXKtmjVIrVSj5bjP-CSTYKdFPbb491tt1IlxMnj0e89zcxD6D3gY8C4OtGdPq4oBfoCzYARKEVF5Us0w6SmJQNCD9CblO4wxrIG_BodVEzUkjA6Q1fforPBjKH7XujOFmN0evtJuUqpvOjsZJwt7qe2c1E3oQ3juhj7wg2hdUNab1XWDRs69N1b9MrrNrl3D-8huv5ydnN6Xi6vFhen82VpqARaEmFs1RDDQNvaM4qN09ZyQ73wDZHaY1ZJ4A2vjPN5RQFOeO2o8KYxmhyiTzvXH7pVQwwrHdeq10Gdz5dq08PAaEVA3ENmj3bsEPtfk0ujWoVkXNvqzvVTUsAxUMlqxv6P1hKyMxYyox-foXf9FLu88obChHBOyNOcJvYpRef3wwJWm-hUjk5to8vshwfHqVk5uycfs8rAyQ74nS-__reTml_OHy3LnSKk0f3ZK3T8qWpOOFO3lwt1W9_wxWf6VV2Tv_4nsQE</recordid><startdate>201507</startdate><enddate>201507</enddate><creator>Becker, Christel</creator><creator>Bouvier, Elodie</creator><creator>Ghestem, Antoine</creator><creator>Siyoucef, Safia</creator><creator>Claverie, Damien</creator><creator>Camus, Françoise</creator><creator>Bartolomei, Fabrice</creator><creator>Benoliel, Jean-Jacques</creator><creator>Bernard, Christophe</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Wiley</general><scope>BSCLL</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>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-3014-1966</orcidid><orcidid>https://orcid.org/0000-0002-1678-0297</orcidid><orcidid>https://orcid.org/0000-0003-4864-609X</orcidid></search><sort><creationdate>201507</creationdate><title>Predicting and treating stress-Induced vulnerability to epilepsy and depression</title><author>Becker, Christel ; Bouvier, Elodie ; Ghestem, Antoine ; Siyoucef, Safia ; Claverie, Damien ; Camus, Françoise ; Bartolomei, Fabrice ; Benoliel, Jean-Jacques ; Bernard, Christophe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4914-38cd2b3c51ad6f540ceadd7c4f8fb39af052917b72cef00281e8fae48fcbca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Allostasis</topic><topic>Animals</topic><topic>Brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor - drug effects</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Cognition Disorders - metabolism</topic><topic>Cognition Disorders - psychology</topic><topic>Depression - metabolism</topic><topic>Depression - psychology</topic><topic>Disease Models, Animal</topic><topic>Epilepsy</topic><topic>Epilepsy - chemically induced</topic><topic>Epilepsy - metabolism</topic><topic>Epilepsy - psychology</topic><topic>Excitatory Amino Acid Agonists - toxicity</topic><topic>Flavones - pharmacology</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Kainic Acid - toxicity</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Neurons and Cognition</topic><topic>Pituitary-Adrenal System - drug effects</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Social Environment</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - metabolism</topic><topic>Stress, Psychological - metabolism</topic><topic>Stress, Psychological - psychology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Becker, Christel</creatorcontrib><creatorcontrib>Bouvier, Elodie</creatorcontrib><creatorcontrib>Ghestem, Antoine</creatorcontrib><creatorcontrib>Siyoucef, Safia</creatorcontrib><creatorcontrib>Claverie, Damien</creatorcontrib><creatorcontrib>Camus, Françoise</creatorcontrib><creatorcontrib>Bartolomei, Fabrice</creatorcontrib><creatorcontrib>Benoliel, Jean-Jacques</creatorcontrib><creatorcontrib>Bernard, Christophe</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Becker, Christel</au><au>Bouvier, Elodie</au><au>Ghestem, Antoine</au><au>Siyoucef, Safia</au><au>Claverie, Damien</au><au>Camus, Françoise</au><au>Bartolomei, Fabrice</au><au>Benoliel, Jean-Jacques</au><au>Bernard, Christophe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Predicting and treating stress-Induced vulnerability to epilepsy and depression</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2015-07</date><risdate>2015</risdate><volume>78</volume><issue>1</issue><spage>128</spage><epage>136</epage><pages>128-136</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><abstract>Accumulation of stressful events can render individuals susceptible to develop epilepsy and comorbidities. Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depression‐like profile and cognitive deficits. Low serum brain‐derived neurotrophic factor (BDNF) levels measured before SE identified this vulnerable population. Treatment with a BDNF analog before SE prevented the occurrence of comorbidities. Thus, vulnerability to comorbidities after epilepsy onset due to unresolved past stressful events may be predicted and reversed. Ann Neurol 2015;78:128–136</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>25869354</pmid><doi>10.1002/ana.24414</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-3014-1966</orcidid><orcidid>https://orcid.org/0000-0002-1678-0297</orcidid><orcidid>https://orcid.org/0000-0003-4864-609X</orcidid></addata></record> |
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subjects | Allostasis Animals Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - drug effects Brain-Derived Neurotrophic Factor - metabolism Cognition Disorders - metabolism Cognition Disorders - psychology Depression - metabolism Depression - psychology Disease Models, Animal Epilepsy Epilepsy - chemically induced Epilepsy - metabolism Epilepsy - psychology Excitatory Amino Acid Agonists - toxicity Flavones - pharmacology Hypothalamo-Hypophyseal System - drug effects Hypothalamo-Hypophyseal System - metabolism Kainic Acid - toxicity Life Sciences Male Neurons and Cognition Pituitary-Adrenal System - drug effects Pituitary-Adrenal System - metabolism Rats Rats, Sprague-Dawley Social Environment Status Epilepticus - chemically induced Status Epilepticus - metabolism Stress, Psychological - metabolism Stress, Psychological - psychology |
title | Predicting and treating stress-Induced vulnerability to epilepsy and depression |
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