The effect of escitalopram, desipramine, electroconvulsive seizures and lithium on brain-derived neurotrophic factor mRNA and protein expression in the rat brain and the correlation to 5-HT and 5-HIAA levels
The reported increase in brain-derived neurotrophic factor (BDNF) mRNA expression after antidepressant treatment is a cornerstone of the BDNF hypothesis of antidepressant action. However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parall...
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description | The reported increase in brain-derived neurotrophic factor (BDNF) mRNA expression after antidepressant treatment is a cornerstone of the BDNF hypothesis of antidepressant action. However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram. ECS increased BDNF mRNA and protein in the hippocampus and BDNF protein in the frontal cortex. Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region. Escitalopram did not affect BDNF mRNA expression, but decreased BDNF protein in the frontal cortex and the hippocampus. Lithium increased BDNF protein levels in the hippocampus and frontal cortex, but overall decreased BDNF mRNA expression. Thus, here we report a striking non-correspondence between changes in BDNF mRNA and protein expression induced by the antidepressant treatments and lithium. Further, increased expression of BDNF mRNA or protein was not a common action of the treatments. We also investigated if treatment-induced modulations of the tissue contents of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA), were related to changes in BDNF mRNA or protein expression. No correlation was found. However, all treatments increased 5-HT levels in the hippocampus. |
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However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram. ECS increased BDNF mRNA and protein in the hippocampus and BDNF protein in the frontal cortex. Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region. Escitalopram did not affect BDNF mRNA expression, but decreased BDNF protein in the frontal cortex and the hippocampus. Lithium increased BDNF protein levels in the hippocampus and frontal cortex, but overall decreased BDNF mRNA expression. Thus, here we report a striking non-correspondence between changes in BDNF mRNA and protein expression induced by the antidepressant treatments and lithium. Further, increased expression of BDNF mRNA or protein was not a common action of the treatments. We also investigated if treatment-induced modulations of the tissue contents of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA), were related to changes in BDNF mRNA or protein expression. No correlation was found. However, all treatments increased 5-HT levels in the hippocampus.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2004.07.065</identifier><identifier>PMID: 15451381</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>5-HT ; Animals ; BDNF ; Biological and medical sciences ; Brain - drug effects ; Brain - metabolism ; Brain-Derived Neurotrophic Factor - biosynthesis ; Brain-Derived Neurotrophic Factor - genetics ; Citalopram - pharmacology ; Desipramine ; Desipramine - pharmacology ; ECS ; Electroshock - methods ; Escitalopram ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. 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However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram. ECS increased BDNF mRNA and protein in the hippocampus and BDNF protein in the frontal cortex. Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region. Escitalopram did not affect BDNF mRNA expression, but decreased BDNF protein in the frontal cortex and the hippocampus. Lithium increased BDNF protein levels in the hippocampus and frontal cortex, but overall decreased BDNF mRNA expression. Thus, here we report a striking non-correspondence between changes in BDNF mRNA and protein expression induced by the antidepressant treatments and lithium. Further, increased expression of BDNF mRNA or protein was not a common action of the treatments. We also investigated if treatment-induced modulations of the tissue contents of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA), were related to changes in BDNF mRNA or protein expression. No correlation was found. However, all treatments increased 5-HT levels in the hippocampus.</description><subject>5-HT</subject><subject>Animals</subject><subject>BDNF</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain-Derived Neurotrophic Factor - biosynthesis</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Citalopram - pharmacology</subject><subject>Desipramine</subject><subject>Desipramine - pharmacology</subject><subject>ECS</subject><subject>Electroshock - methods</subject><subject>Escitalopram</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hydroxyindoleacetic Acid - metabolism</subject><subject>Lithium</subject><subject>Lithium - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Seizures - genetics</subject><subject>Seizures - metabolism</subject><subject>Serotonin - biosynthesis</subject><subject>Serotonin - genetics</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAUhSMEoqXwCpU3sGoG2_mxs2NUAa1UgYSGteXY1xqPnHiwk1HhJXklbmYGddmVf-53ro99XBTXjK4YZe3H3apP2o8J8opTWq-oWNG2eVFcMil42fKaviwuKaVtKbuuuije5LzDZVV19HVxwZq6YZVkl8XfzRYIOAdmItERyMZPOsR90sMNsZD9MvMj3BAIyKRo4niYQ_YHIBn8nxkdED1aEvy09fNA4kiOzkoLCSFLRphTROF-6w1x2kwxkeHHt_VRtccS-JHA4x4bZY9qXE3oKenp1OjILTsmpgRBTws0RdKUd5tjDSf36zUJcICQ3xavnA4Z3p3Hq-Lnl8-b27vy4fvX-9v1Q2nqjk2lA9dLqHsuRC-Mc1a0Hb4fNX1fc-B9xSuopHRM8t62vAHNhbG9rK0EFNLqqvhw6os3-DVDntTgs4EQ9AhxzqptO1YJUT0LMlFLKRqOYHsCTYo5J3Bqn_yg02_FqFoyVzv1P3O1ZK6oUOgZhdfnE-Z-APskO4eMwPszoLPRwSU9Gp-fuJY1sqOL1U8nDt8RDh6Swt8AowHrE2avbPTPefkHgPTSpQ</recordid><startdate>20041022</startdate><enddate>20041022</enddate><creator>Jacobsen, Jacob Pade Ramsøe</creator><creator>Mørk, Arne</creator><general>Elsevier B.V</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20041022</creationdate><title>The effect of escitalopram, desipramine, electroconvulsive seizures and lithium on brain-derived neurotrophic factor mRNA and protein expression in the rat brain and the correlation to 5-HT and 5-HIAA levels</title><author>Jacobsen, Jacob Pade Ramsøe ; Mørk, Arne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-fefb8e4b277b7cffd7690650cbb42e2b323e388f182bd625ea27cdb84d8eb8e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>5-HT</topic><topic>Animals</topic><topic>BDNF</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Brain-Derived Neurotrophic Factor - biosynthesis</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Citalopram - pharmacology</topic><topic>Desipramine</topic><topic>Desipramine - pharmacology</topic><topic>ECS</topic><topic>Electroshock - methods</topic><topic>Escitalopram</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hydroxyindoleacetic Acid - metabolism</topic><topic>Lithium</topic><topic>Lithium - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Seizures - genetics</topic><topic>Seizures - metabolism</topic><topic>Serotonin - biosynthesis</topic><topic>Serotonin - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jacobsen, Jacob Pade Ramsøe</creatorcontrib><creatorcontrib>Mørk, Arne</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jacobsen, Jacob Pade Ramsøe</au><au>Mørk, Arne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of escitalopram, desipramine, electroconvulsive seizures and lithium on brain-derived neurotrophic factor mRNA and protein expression in the rat brain and the correlation to 5-HT and 5-HIAA levels</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2004-10-22</date><risdate>2004</risdate><volume>1024</volume><issue>1</issue><spage>183</spage><epage>192</epage><pages>183-192</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>The reported increase in brain-derived neurotrophic factor (BDNF) mRNA expression after antidepressant treatment is a cornerstone of the BDNF hypothesis of antidepressant action. However, if this increase becomes manifest on the BDNF protein level is unknown. In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram. ECS increased BDNF mRNA and protein in the hippocampus and BDNF protein in the frontal cortex. Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region. Escitalopram did not affect BDNF mRNA expression, but decreased BDNF protein in the frontal cortex and the hippocampus. Lithium increased BDNF protein levels in the hippocampus and frontal cortex, but overall decreased BDNF mRNA expression. Thus, here we report a striking non-correspondence between changes in BDNF mRNA and protein expression induced by the antidepressant treatments and lithium. Further, increased expression of BDNF mRNA or protein was not a common action of the treatments. We also investigated if treatment-induced modulations of the tissue contents of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxy-indoleacetic acid (5-HIAA), were related to changes in BDNF mRNA or protein expression. No correlation was found. However, all treatments increased 5-HT levels in the hippocampus.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>15451381</pmid><doi>10.1016/j.brainres.2004.07.065</doi><tpages>10</tpages></addata></record> |
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subjects | 5-HT Animals BDNF Biological and medical sciences Brain - drug effects Brain - metabolism Brain-Derived Neurotrophic Factor - biosynthesis Brain-Derived Neurotrophic Factor - genetics Citalopram - pharmacology Desipramine Desipramine - pharmacology ECS Electroshock - methods Escitalopram Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hydroxyindoleacetic Acid - metabolism Lithium Lithium - pharmacology Male Medical sciences Nervous system (semeiology, syndromes) Neurology Proteins - genetics Proteins - metabolism Rats Rats, Wistar RNA, Messenger - biosynthesis RNA, Messenger - genetics Seizures - genetics Seizures - metabolism Serotonin - biosynthesis Serotonin - genetics |
title | The effect of escitalopram, desipramine, electroconvulsive seizures and lithium on brain-derived neurotrophic factor mRNA and protein expression in the rat brain and the correlation to 5-HT and 5-HIAA levels |
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