Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants
Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases. Converging evidence suggested that acute stress is associated with increase of excitatory transmission in certain forebrain areas. Aim of this work was to investigate the mechanism whereby acute stress increases glu...
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| Veröffentlicht in: | PloS one 2010-01, Vol.5 (1), p.e8566 |
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| creator | Musazzi, Laura Milanese, Marco Farisello, Pasqualina Zappettini, Simona Tardito, Daniela Barbiero, Valentina S Bonifacino, Tiziana Mallei, Alessandra Baldelli, Pietro Racagni, Giorgio Raiteri, Maurizio Benfenati, Fabio Bonanno, Giambattista Popoli, Maurizio |
| description | Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases. Converging evidence suggested that acute stress is associated with increase of excitatory transmission in certain forebrain areas. Aim of this work was to investigate the mechanism whereby acute stress increases glutamate release, and if therapeutic drugs prevent the effect of stress on glutamate release.
Rats were chronically treated with vehicle or drugs employed for therapy of mood/anxiety disorders (fluoxetine, desipramine, venlafaxine, agomelatine) and then subjected to unpredictable footshock stress. Acute stress induced marked increase in depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex in superfusion, and the chronic drug treatments prevented the increase of glutamate release. Stress induced rapid increase in the circulating levels of corticosterone in all rats (both vehicle- and drug-treated), and glutamate release increase was blocked by previous administration of selective antagonist of glucocorticoid receptor (RU 486). On the molecular level, stress induced accumulation of presynaptic SNARE complexes in synaptic membranes (both in vehicle- and drug-treated rats). Patch-clamp recordings of pyramidal neurons in the prefrontal cortex revealed that stress increased glutamatergic transmission through both pre- and postsynaptic mechanisms, and that antidepressants may normalize it by reducing release probability.
Acute footshock stress up-regulated depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex. Stress-induced increase of glutamate release was dependent on stimulation of glucocorticoid receptor by corticosterone. Because all drugs employed did not block either elevation of corticosterone or accumulation of SNARE complexes, the dampening action of the drugs on glutamate release must be downstream of these processes. This novel effect of antidepressants on the response to stress, shown here for the first time, could be related to the therapeutic action of these drugs. |
| doi_str_mv | 10.1371/journal.pone.0008566 |
| format | Article |
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Rats were chronically treated with vehicle or drugs employed for therapy of mood/anxiety disorders (fluoxetine, desipramine, venlafaxine, agomelatine) and then subjected to unpredictable footshock stress. Acute stress induced marked increase in depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex in superfusion, and the chronic drug treatments prevented the increase of glutamate release. Stress induced rapid increase in the circulating levels of corticosterone in all rats (both vehicle- and drug-treated), and glutamate release increase was blocked by previous administration of selective antagonist of glucocorticoid receptor (RU 486). On the molecular level, stress induced accumulation of presynaptic SNARE complexes in synaptic membranes (both in vehicle- and drug-treated rats). Patch-clamp recordings of pyramidal neurons in the prefrontal cortex revealed that stress increased glutamatergic transmission through both pre- and postsynaptic mechanisms, and that antidepressants may normalize it by reducing release probability.
Acute footshock stress up-regulated depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex. Stress-induced increase of glutamate release was dependent on stimulation of glucocorticoid receptor by corticosterone. Because all drugs employed did not block either elevation of corticosterone or accumulation of SNARE complexes, the dampening action of the drugs on glutamate release must be downstream of these processes. This novel effect of antidepressants on the response to stress, shown here for the first time, could be related to the therapeutic action of these drugs.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0008566</identifier><identifier>PMID: 20052403</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Amino acids ; Animals ; Antidepressants ; Antidepressive Agents - pharmacology ; Antidepressive Agents - therapeutic use ; Anxiety ; Biomedical research ; Brain research ; Cortex (frontal) ; Corticosterone ; Corticosterone - metabolism ; Depolarization ; Desipramine ; Disease transmission ; Downstream effects ; Drug delivery ; Drugs ; Fluoxetine ; Footshock ; Forebrain ; Frontal Lobe - drug effects ; Frontal Lobe - metabolism ; Frontal Lobe - physiopathology ; Glucocorticoids ; Glutamate ; Glutamatergic transmission ; Glutamic Acid - metabolism ; Health aspects ; Health risks ; Kinases ; Medicine ; Melatonin ; Membranes ; Mental disorders ; Mental Health/Neuropsychiatric Disorders ; Mental Health/Psychopharmacology ; Mood ; Neurological Disorders/Neuropharmacology ; Neurological Disorders/Neuropsychiatric Disorders ; Neurons ; Neurosciences ; Pharmacology ; Phosphorylation ; Physiology ; Prefrontal cortex ; Protein expression ; Pyramidal cells ; Rats ; Receptors, Glucocorticoid - metabolism ; Risk factors ; Risk taking ; Rodents ; Schizophrenia ; SNAP receptors ; SNARE Proteins - metabolism ; Stress ; Stress response ; Stress, Psychological - drug therapy ; Stresses ; Synaptic membranes ; Synaptosomes ; Toxicology ; Venlafaxine</subject><ispartof>PloS one, 2010-01, Vol.5 (1), p.e8566</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Musazzi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Musazzi et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c789t-d7aa1aabfca1424412001569ba9cc471ea6c60d45e857c235afd16f3e20f15d23</citedby><cites>FETCH-LOGICAL-c789t-d7aa1aabfca1424412001569ba9cc471ea6c60d45e857c235afd16f3e20f15d23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797327/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797327/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2104,2930,23873,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20052403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bartolomucci, Alessandro</contributor><creatorcontrib>Musazzi, Laura</creatorcontrib><creatorcontrib>Milanese, Marco</creatorcontrib><creatorcontrib>Farisello, Pasqualina</creatorcontrib><creatorcontrib>Zappettini, Simona</creatorcontrib><creatorcontrib>Tardito, Daniela</creatorcontrib><creatorcontrib>Barbiero, Valentina S</creatorcontrib><creatorcontrib>Bonifacino, Tiziana</creatorcontrib><creatorcontrib>Mallei, Alessandra</creatorcontrib><creatorcontrib>Baldelli, Pietro</creatorcontrib><creatorcontrib>Racagni, Giorgio</creatorcontrib><creatorcontrib>Raiteri, Maurizio</creatorcontrib><creatorcontrib>Benfenati, Fabio</creatorcontrib><creatorcontrib>Bonanno, Giambattista</creatorcontrib><creatorcontrib>Popoli, Maurizio</creatorcontrib><title>Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases. Converging evidence suggested that acute stress is associated with increase of excitatory transmission in certain forebrain areas. Aim of this work was to investigate the mechanism whereby acute stress increases glutamate release, and if therapeutic drugs prevent the effect of stress on glutamate release.
Rats were chronically treated with vehicle or drugs employed for therapy of mood/anxiety disorders (fluoxetine, desipramine, venlafaxine, agomelatine) and then subjected to unpredictable footshock stress. Acute stress induced marked increase in depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex in superfusion, and the chronic drug treatments prevented the increase of glutamate release. Stress induced rapid increase in the circulating levels of corticosterone in all rats (both vehicle- and drug-treated), and glutamate release increase was blocked by previous administration of selective antagonist of glucocorticoid receptor (RU 486). On the molecular level, stress induced accumulation of presynaptic SNARE complexes in synaptic membranes (both in vehicle- and drug-treated rats). Patch-clamp recordings of pyramidal neurons in the prefrontal cortex revealed that stress increased glutamatergic transmission through both pre- and postsynaptic mechanisms, and that antidepressants may normalize it by reducing release probability.
Acute footshock stress up-regulated depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex. Stress-induced increase of glutamate release was dependent on stimulation of glucocorticoid receptor by corticosterone. Because all drugs employed did not block either elevation of corticosterone or accumulation of SNARE complexes, the dampening action of the drugs on glutamate release must be downstream of these processes. This novel effect of antidepressants on the response to stress, shown here for the first time, could be related to the therapeutic action of these drugs.</description><subject>Accumulation</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Antidepressive Agents - therapeutic use</subject><subject>Anxiety</subject><subject>Biomedical research</subject><subject>Brain research</subject><subject>Cortex (frontal)</subject><subject>Corticosterone</subject><subject>Corticosterone - metabolism</subject><subject>Depolarization</subject><subject>Desipramine</subject><subject>Disease transmission</subject><subject>Downstream effects</subject><subject>Drug delivery</subject><subject>Drugs</subject><subject>Fluoxetine</subject><subject>Footshock</subject><subject>Forebrain</subject><subject>Frontal Lobe - drug effects</subject><subject>Frontal Lobe - metabolism</subject><subject>Frontal Lobe - physiopathology</subject><subject>Glucocorticoids</subject><subject>Glutamate</subject><subject>Glutamatergic transmission</subject><subject>Glutamic Acid - metabolism</subject><subject>Health aspects</subject><subject>Health risks</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Melatonin</subject><subject>Membranes</subject><subject>Mental disorders</subject><subject>Mental Health/Neuropsychiatric Disorders</subject><subject>Mental Health/Psychopharmacology</subject><subject>Mood</subject><subject>Neurological Disorders/Neuropharmacology</subject><subject>Neurological Disorders/Neuropsychiatric Disorders</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Pharmacology</subject><subject>Phosphorylation</subject><subject>Physiology</subject><subject>Prefrontal cortex</subject><subject>Protein expression</subject><subject>Pyramidal cells</subject><subject>Rats</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>Risk factors</subject><subject>Risk taking</subject><subject>Rodents</subject><subject>Schizophrenia</subject><subject>SNAP receptors</subject><subject>SNARE Proteins - metabolism</subject><subject>Stress</subject><subject>Stress response</subject><subject>Stress, Psychological - drug therapy</subject><subject>Stresses</subject><subject>Synaptic membranes</subject><subject>Synaptosomes</subject><subject>Toxicology</subject><subject>Venlafaxine</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk22L1DAQx4so3nn6DUQLguKL3Wue2sYXwnL4sHBw4NPbMJtOu1nbZi9JD_Uz-KFNb3vHrhwohWaS_uY_nclMkjwl2Zywgpxu7OB6aOdb2-M8y7JS5Pm95JhIRmc5zdj9PfsoeeT9JssEK_P8YXJEo0l5xo6T3ws9BEx9cOh9anrtEDz6tMKtbcGZXxCM7Wd4Zb9jlTbtEKCD6OCwHcHokYZ13EJItw5rZ_sA7em0ptq6gD_eXCMVdFvsTd-koEfN1NYp9MHESGPsaPrHyYMaWo9PpvUk-fr-3Zezj7Pziw_Ls8X5TBelDLOqACAAq1oD4ZRzEtMhIpcrkFrzgiDkOs8qLrAUhaZMQF2RvGZIs5qIirKT5PlOd9tar6ZCekVoKakgkpaRWO6IysJGbZ3pwP1UFoy6PrCuUeCC0S2qjEskVcmpoBhfWDItWFFUOa1LKQWLWm-naMOqw0pjHxy0B6KHX3qzVo29UrSQBaNFFHg1CTh7OaAPqjNeY9tCj3bwquA8l6UQ8t8kY4JTUvJIvviLvLsME9VAzNT0tY0_qEdNteAFk5RwPiY4v4OKT4Wd0bE9axPPDxxeHzhEJrZJaGDwXi0_f_p_9uLbIftyj10jtGHtbezZ2G7-EOQ7UDvrfezb29sgmRqn66YaapwuNU1XdHu2f5O3TjfjxP4ATBohfw</recordid><startdate>20100105</startdate><enddate>20100105</enddate><creator>Musazzi, Laura</creator><creator>Milanese, Marco</creator><creator>Farisello, Pasqualina</creator><creator>Zappettini, Simona</creator><creator>Tardito, Daniela</creator><creator>Barbiero, Valentina S</creator><creator>Bonifacino, Tiziana</creator><creator>Mallei, Alessandra</creator><creator>Baldelli, Pietro</creator><creator>Racagni, Giorgio</creator><creator>Raiteri, Maurizio</creator><creator>Benfenati, Fabio</creator><creator>Bonanno, Giambattista</creator><creator>Popoli, Maurizio</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20100105</creationdate><title>Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants</title><author>Musazzi, Laura ; Milanese, Marco ; Farisello, Pasqualina ; Zappettini, Simona ; Tardito, Daniela ; Barbiero, Valentina S ; Bonifacino, Tiziana ; Mallei, Alessandra ; Baldelli, Pietro ; Racagni, Giorgio ; Raiteri, Maurizio ; Benfenati, Fabio ; Bonanno, Giambattista ; Popoli, Maurizio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c789t-d7aa1aabfca1424412001569ba9cc471ea6c60d45e857c235afd16f3e20f15d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Accumulation</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Antidepressive Agents - 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metabolism</topic><topic>Risk factors</topic><topic>Risk taking</topic><topic>Rodents</topic><topic>Schizophrenia</topic><topic>SNAP receptors</topic><topic>SNARE Proteins - metabolism</topic><topic>Stress</topic><topic>Stress response</topic><topic>Stress, Psychological - drug therapy</topic><topic>Stresses</topic><topic>Synaptic membranes</topic><topic>Synaptosomes</topic><topic>Toxicology</topic><topic>Venlafaxine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Musazzi, Laura</creatorcontrib><creatorcontrib>Milanese, Marco</creatorcontrib><creatorcontrib>Farisello, Pasqualina</creatorcontrib><creatorcontrib>Zappettini, Simona</creatorcontrib><creatorcontrib>Tardito, Daniela</creatorcontrib><creatorcontrib>Barbiero, Valentina S</creatorcontrib><creatorcontrib>Bonifacino, Tiziana</creatorcontrib><creatorcontrib>Mallei, Alessandra</creatorcontrib><creatorcontrib>Baldelli, Pietro</creatorcontrib><creatorcontrib>Racagni, Giorgio</creatorcontrib><creatorcontrib>Raiteri, Maurizio</creatorcontrib><creatorcontrib>Benfenati, Fabio</creatorcontrib><creatorcontrib>Bonanno, Giambattista</creatorcontrib><creatorcontrib>Popoli, Maurizio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Musazzi, Laura</au><au>Milanese, Marco</au><au>Farisello, Pasqualina</au><au>Zappettini, Simona</au><au>Tardito, Daniela</au><au>Barbiero, Valentina S</au><au>Bonifacino, Tiziana</au><au>Mallei, Alessandra</au><au>Baldelli, Pietro</au><au>Racagni, Giorgio</au><au>Raiteri, Maurizio</au><au>Benfenati, Fabio</au><au>Bonanno, Giambattista</au><au>Popoli, Maurizio</au><au>Bartolomucci, Alessandro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-01-05</date><risdate>2010</risdate><volume>5</volume><issue>1</issue><spage>e8566</spage><pages>e8566-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Behavioral stress is recognized as a main risk factor for neuropsychiatric diseases. Converging evidence suggested that acute stress is associated with increase of excitatory transmission in certain forebrain areas. Aim of this work was to investigate the mechanism whereby acute stress increases glutamate release, and if therapeutic drugs prevent the effect of stress on glutamate release.
Rats were chronically treated with vehicle or drugs employed for therapy of mood/anxiety disorders (fluoxetine, desipramine, venlafaxine, agomelatine) and then subjected to unpredictable footshock stress. Acute stress induced marked increase in depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex in superfusion, and the chronic drug treatments prevented the increase of glutamate release. Stress induced rapid increase in the circulating levels of corticosterone in all rats (both vehicle- and drug-treated), and glutamate release increase was blocked by previous administration of selective antagonist of glucocorticoid receptor (RU 486). On the molecular level, stress induced accumulation of presynaptic SNARE complexes in synaptic membranes (both in vehicle- and drug-treated rats). Patch-clamp recordings of pyramidal neurons in the prefrontal cortex revealed that stress increased glutamatergic transmission through both pre- and postsynaptic mechanisms, and that antidepressants may normalize it by reducing release probability.
Acute footshock stress up-regulated depolarization-evoked release of glutamate from synaptosomes of prefrontal/frontal cortex. Stress-induced increase of glutamate release was dependent on stimulation of glucocorticoid receptor by corticosterone. Because all drugs employed did not block either elevation of corticosterone or accumulation of SNARE complexes, the dampening action of the drugs on glutamate release must be downstream of these processes. This novel effect of antidepressants on the response to stress, shown here for the first time, could be related to the therapeutic action of these drugs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20052403</pmid><doi>10.1371/journal.pone.0008566</doi><tpages>e8566</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2010-01, Vol.5 (1), p.e8566 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1289251928 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Accumulation Amino acids Animals Antidepressants Antidepressive Agents - pharmacology Antidepressive Agents - therapeutic use Anxiety Biomedical research Brain research Cortex (frontal) Corticosterone Corticosterone - metabolism Depolarization Desipramine Disease transmission Downstream effects Drug delivery Drugs Fluoxetine Footshock Forebrain Frontal Lobe - drug effects Frontal Lobe - metabolism Frontal Lobe - physiopathology Glucocorticoids Glutamate Glutamatergic transmission Glutamic Acid - metabolism Health aspects Health risks Kinases Medicine Melatonin Membranes Mental disorders Mental Health/Neuropsychiatric Disorders Mental Health/Psychopharmacology Mood Neurological Disorders/Neuropharmacology Neurological Disorders/Neuropsychiatric Disorders Neurons Neurosciences Pharmacology Phosphorylation Physiology Prefrontal cortex Protein expression Pyramidal cells Rats Receptors, Glucocorticoid - metabolism Risk factors Risk taking Rodents Schizophrenia SNAP receptors SNARE Proteins - metabolism Stress Stress response Stress, Psychological - drug therapy Stresses Synaptic membranes Synaptosomes Toxicology Venlafaxine |
| title | Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants |
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