Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype
Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs. However, the relationship between BDNF and serotonergic signalling is poorly understood. Heterozygous mutants BDNF +/− mice were utilized to in...
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| Veröffentlicht in: | The international journal of neuropsychopharmacology 2008-02, Vol.11 (1), p.79-92 |
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| creator | Guiard, Bruno P. David, Denis J. P. Deltheil, Thierry Chenu, Franck Le Maître, Erwan Renoir, Thibault Leroux-Nicollet, Isabelle Sokoloff, Pierre Lanfumey, Laurence Hamon, Michel Andrews, Anne M. Hen, René Gardier, Alain M. |
| description | Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs. However, the relationship between BDNF and serotonergic signalling is poorly understood. Heterozygous mutants BDNF +/− mice were utilized to investigate the influence of BDNF on the serotonin (5-HT) system and the activity of the serotonin transporter (SERT) in the hippocampus. The zero net flux method of quantitative microdialysis revealed that BDNF +/− heterozygous mice have increased basal extracellular 5-HT levels in the hippocampus and decreased 5-HT reuptake capacity. In keeping with these results, the selective serotonin reuptake inhibitor paroxetine failed to increase hippocampal extracellular 5-HT levels in BDNF +/− mice while it produced robust effects in wild-type littermates. Using in-vitro autoradiography and synaptosome techniques, we investigated the causes of attenuated 5-HT reuptake in BDNF +/− mice. A significant decrease in [3H]citalopram-binding-site density in the CA3 subregion of the ventral hippocampus and a significant reduction in [3H]5-HT uptake in hippocampal synaptosomes, revealed mainly a decrease in SERT function. However, 5-HT1A autoreceptors were not desensitized in BDNF +/− mice. These results provide evidence that constitutive reductions in BDNF modulate SERT function reuptake in the hippocampus. |
| doi_str_mv | 10.1017/S1461145707007857 |
| format | Article |
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P. ; Deltheil, Thierry ; Chenu, Franck ; Le Maître, Erwan ; Renoir, Thibault ; Leroux-Nicollet, Isabelle ; Sokoloff, Pierre ; Lanfumey, Laurence ; Hamon, Michel ; Andrews, Anne M. ; Hen, René ; Gardier, Alain M.</creator><creatorcontrib>Guiard, Bruno P. ; David, Denis J. P. ; Deltheil, Thierry ; Chenu, Franck ; Le Maître, Erwan ; Renoir, Thibault ; Leroux-Nicollet, Isabelle ; Sokoloff, Pierre ; Lanfumey, Laurence ; Hamon, Michel ; Andrews, Anne M. ; Hen, René ; Gardier, Alain M.</creatorcontrib><description>Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs. However, the relationship between BDNF and serotonergic signalling is poorly understood. Heterozygous mutants BDNF +/− mice were utilized to investigate the influence of BDNF on the serotonin (5-HT) system and the activity of the serotonin transporter (SERT) in the hippocampus. The zero net flux method of quantitative microdialysis revealed that BDNF +/− heterozygous mice have increased basal extracellular 5-HT levels in the hippocampus and decreased 5-HT reuptake capacity. In keeping with these results, the selective serotonin reuptake inhibitor paroxetine failed to increase hippocampal extracellular 5-HT levels in BDNF +/− mice while it produced robust effects in wild-type littermates. Using in-vitro autoradiography and synaptosome techniques, we investigated the causes of attenuated 5-HT reuptake in BDNF +/− mice. A significant decrease in [3H]citalopram-binding-site density in the CA3 subregion of the ventral hippocampus and a significant reduction in [3H]5-HT uptake in hippocampal synaptosomes, revealed mainly a decrease in SERT function. However, 5-HT1A autoreceptors were not desensitized in BDNF +/− mice. These results provide evidence that constitutive reductions in BDNF modulate SERT function reuptake in the hippocampus.</description><identifier>ISSN: 1461-1457</identifier><identifier>EISSN: 1469-5111</identifier><identifier>DOI: 10.1017/S1461145707007857</identifier><identifier>PMID: 17559709</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology ; Animals ; Autoradiography ; Brain ; Brain Chemistry - drug effects ; Brain-Derived Neurotrophic Factor - deficiency ; Brain-Derived Neurotrophic Factor - genetics ; Changes ; Citalopram ; Dose-Response Relationship, Drug ; Electrophysiology ; Gene loci ; Hippocampus - drug effects ; Hippocampus - metabolism ; Male ; Mice ; Mice, Knockout ; Microdialysis ; Paroxetine ; Phenotype ; Raphe Nuclei - drug effects ; Raphe Nuclei - metabolism ; Receptor, Serotonin, 5-HT1A - drug effects ; Receptor, Serotonin, 5-HT1A - metabolism ; Serotonin - metabolism ; Serotonin Plasma Membrane Transport Proteins - metabolism ; Serotonin Receptor Agonists - pharmacology ; Serotonin Uptake Inhibitors ; Studies ; Synaptic Transmission - genetics ; Synaptic Transmission - physiology ; Temperature</subject><ispartof>The international journal of neuropsychopharmacology, 2008-02, Vol.11 (1), p.79-92</ispartof><rights>Copyright © Collegium Internationale Neuropsychopharmacologicum 2007</rights><rights>Copyright © Collegium Internationale Neuropsychopharmacologicum 2007 2007</rights><rights>Copyright Cambridge University Press Feb 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-b2c928a13cffdd0ea745613c666e59f82a74777a2d2eaf12f60877f2d87fbc023</citedby><cites>FETCH-LOGICAL-c450t-b2c928a13cffdd0ea745613c666e59f82a74777a2d2eaf12f60877f2d87fbc023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17559709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guiard, Bruno P.</creatorcontrib><creatorcontrib>David, Denis J. P.</creatorcontrib><creatorcontrib>Deltheil, Thierry</creatorcontrib><creatorcontrib>Chenu, Franck</creatorcontrib><creatorcontrib>Le Maître, Erwan</creatorcontrib><creatorcontrib>Renoir, Thibault</creatorcontrib><creatorcontrib>Leroux-Nicollet, Isabelle</creatorcontrib><creatorcontrib>Sokoloff, Pierre</creatorcontrib><creatorcontrib>Lanfumey, Laurence</creatorcontrib><creatorcontrib>Hamon, Michel</creatorcontrib><creatorcontrib>Andrews, Anne M.</creatorcontrib><creatorcontrib>Hen, René</creatorcontrib><creatorcontrib>Gardier, Alain M.</creatorcontrib><title>Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype</title><title>The international journal of neuropsychopharmacology</title><addtitle>Int J Neuropsychopharmacol</addtitle><description>Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs. However, the relationship between BDNF and serotonergic signalling is poorly understood. Heterozygous mutants BDNF +/− mice were utilized to investigate the influence of BDNF on the serotonin (5-HT) system and the activity of the serotonin transporter (SERT) in the hippocampus. The zero net flux method of quantitative microdialysis revealed that BDNF +/− heterozygous mice have increased basal extracellular 5-HT levels in the hippocampus and decreased 5-HT reuptake capacity. In keeping with these results, the selective serotonin reuptake inhibitor paroxetine failed to increase hippocampal extracellular 5-HT levels in BDNF +/− mice while it produced robust effects in wild-type littermates. Using in-vitro autoradiography and synaptosome techniques, we investigated the causes of attenuated 5-HT reuptake in BDNF +/− mice. A significant decrease in [3H]citalopram-binding-site density in the CA3 subregion of the ventral hippocampus and a significant reduction in [3H]5-HT uptake in hippocampal synaptosomes, revealed mainly a decrease in SERT function. However, 5-HT1A autoreceptors were not desensitized in BDNF +/− mice. These results provide evidence that constitutive reductions in BDNF modulate SERT function reuptake in the hippocampus.</description><subject>8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology</subject><subject>Animals</subject><subject>Autoradiography</subject><subject>Brain</subject><subject>Brain Chemistry - drug effects</subject><subject>Brain-Derived Neurotrophic Factor - deficiency</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Changes</subject><subject>Citalopram</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electrophysiology</subject><subject>Gene loci</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microdialysis</subject><subject>Paroxetine</subject><subject>Phenotype</subject><subject>Raphe Nuclei - drug effects</subject><subject>Raphe Nuclei - metabolism</subject><subject>Receptor, Serotonin, 5-HT1A - drug effects</subject><subject>Receptor, Serotonin, 5-HT1A - metabolism</subject><subject>Serotonin - metabolism</subject><subject>Serotonin Plasma Membrane Transport Proteins - metabolism</subject><subject>Serotonin Receptor Agonists - pharmacology</subject><subject>Serotonin Uptake Inhibitors</subject><subject>Studies</subject><subject>Synaptic Transmission - genetics</subject><subject>Synaptic Transmission - physiology</subject><subject>Temperature</subject><issn>1461-1457</issn><issn>1469-5111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNUE1LxDAUDKL4_QO8SPHgyepL2jTtUcUvEDyo55KmL9vItolJK_rvje7CgiIYCHmZNzMMQ8gBhVMKVJw90rygNOcCBIAouVgj2xGqUk4pXf-eafq13yI7IbwAsJxnxSbZooLzSkC1TZoLL82QtujNG7bJgJO3o7euMyrRUo3Wx502yuAwJr1RmOB7ZxozJjLpjHNWyd7JedJ9OPQBo9gO6GdR7Toc7BjhPbKh5Tzg_vLdJc_XV0-Xt-n9w83d5fl9qnIOY9owVbFS0kxp3baAUuS8iL-iKJBXumQREEJI1jKUmjJdQCmEZm0pdKOAZbvkeOHrvH2dMIx1b4LC-VwOaKdQC2BAMxCRePSD-GInP8RsNYunhHgjiS5IytsQPOraedNL_1FTqL_ar3-1HzWHS-Op6bFdKZZ1R8LJgmAn9y-_bJlB9o037QxXSf9WfQLhbJzS</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Guiard, Bruno P.</creator><creator>David, Denis J. 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P. ; Deltheil, Thierry ; Chenu, Franck ; Le Maître, Erwan ; Renoir, Thibault ; Leroux-Nicollet, Isabelle ; Sokoloff, Pierre ; Lanfumey, Laurence ; Hamon, Michel ; Andrews, Anne M. ; Hen, René ; Gardier, Alain M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-b2c928a13cffdd0ea745613c666e59f82a74777a2d2eaf12f60877f2d87fbc023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology</topic><topic>Animals</topic><topic>Autoradiography</topic><topic>Brain</topic><topic>Brain Chemistry - drug effects</topic><topic>Brain-Derived Neurotrophic Factor - deficiency</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Changes</topic><topic>Citalopram</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electrophysiology</topic><topic>Gene loci</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microdialysis</topic><topic>Paroxetine</topic><topic>Phenotype</topic><topic>Raphe Nuclei - drug effects</topic><topic>Raphe Nuclei - metabolism</topic><topic>Receptor, Serotonin, 5-HT1A - drug effects</topic><topic>Receptor, Serotonin, 5-HT1A - metabolism</topic><topic>Serotonin - metabolism</topic><topic>Serotonin Plasma Membrane Transport Proteins - metabolism</topic><topic>Serotonin Receptor Agonists - pharmacology</topic><topic>Serotonin Uptake Inhibitors</topic><topic>Studies</topic><topic>Synaptic Transmission - genetics</topic><topic>Synaptic Transmission - physiology</topic><topic>Temperature</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guiard, Bruno P.</creatorcontrib><creatorcontrib>David, Denis J. 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P.</au><au>Deltheil, Thierry</au><au>Chenu, Franck</au><au>Le Maître, Erwan</au><au>Renoir, Thibault</au><au>Leroux-Nicollet, Isabelle</au><au>Sokoloff, Pierre</au><au>Lanfumey, Laurence</au><au>Hamon, Michel</au><au>Andrews, Anne M.</au><au>Hen, René</au><au>Gardier, Alain M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype</atitle><jtitle>The international journal of neuropsychopharmacology</jtitle><addtitle>Int J Neuropsychopharmacol</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>11</volume><issue>1</issue><spage>79</spage><epage>92</epage><pages>79-92</pages><issn>1461-1457</issn><eissn>1469-5111</eissn><abstract>Growing evidence supports the involvement of brain-derived neurotrophic factor (BDNF) in mood disorders and the mechanism of action of antidepressant drugs. However, the relationship between BDNF and serotonergic signalling is poorly understood. Heterozygous mutants BDNF +/− mice were utilized to investigate the influence of BDNF on the serotonin (5-HT) system and the activity of the serotonin transporter (SERT) in the hippocampus. The zero net flux method of quantitative microdialysis revealed that BDNF +/− heterozygous mice have increased basal extracellular 5-HT levels in the hippocampus and decreased 5-HT reuptake capacity. In keeping with these results, the selective serotonin reuptake inhibitor paroxetine failed to increase hippocampal extracellular 5-HT levels in BDNF +/− mice while it produced robust effects in wild-type littermates. Using in-vitro autoradiography and synaptosome techniques, we investigated the causes of attenuated 5-HT reuptake in BDNF +/− mice. A significant decrease in [3H]citalopram-binding-site density in the CA3 subregion of the ventral hippocampus and a significant reduction in [3H]5-HT uptake in hippocampal synaptosomes, revealed mainly a decrease in SERT function. However, 5-HT1A autoreceptors were not desensitized in BDNF +/− mice. These results provide evidence that constitutive reductions in BDNF modulate SERT function reuptake in the hippocampus.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>17559709</pmid><doi>10.1017/S1461145707007857</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology Animals Autoradiography Brain Brain Chemistry - drug effects Brain-Derived Neurotrophic Factor - deficiency Brain-Derived Neurotrophic Factor - genetics Changes Citalopram Dose-Response Relationship, Drug Electrophysiology Gene loci Hippocampus - drug effects Hippocampus - metabolism Male Mice Mice, Knockout Microdialysis Paroxetine Phenotype Raphe Nuclei - drug effects Raphe Nuclei - metabolism Receptor, Serotonin, 5-HT1A - drug effects Receptor, Serotonin, 5-HT1A - metabolism Serotonin - metabolism Serotonin Plasma Membrane Transport Proteins - metabolism Serotonin Receptor Agonists - pharmacology Serotonin Uptake Inhibitors Studies Synaptic Transmission - genetics Synaptic Transmission - physiology Temperature |
| title | Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype |
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