Changes in AMPA subunit expression in the mouse brain after chronic treatment with the antidepressant maprotiline : a link between noradrenergic and glutamatergic function?
Potentiation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function has been proposed as being useful in the treatment of depression, but thus far, little is known about the possible changes in AMPA receptor expression in the brain, after antidepressant treatment. The p...
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description | Potentiation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function has been proposed as being useful in the treatment of depression, but thus far, little is known about the possible changes in AMPA receptor expression in the brain, after antidepressant treatment. The present study was carried out to study the expression of AMPA receptor subunits in different brain regions of mice that had been chronically injected with maprotiline. The latter is a modified tricyclic antidepressant that functions as a noradrenaline uptake inhibitor. Daily intraperitoneal injection with 10 mg/kg maprotiline for 30 days resulted in significantly increased GluR1 and GluR2/3 subunit expression in the nucleus accumbens and dorsal striatum as detected by immunohistochemistry; and significantly increased GluR1 and GluR2/3 expression in the hippocampus, as demonstrated by Western blot analysis. No change, or a decrease in GluR2 expression was detected in all the brain regions by both immunohistochemistry and Western blots. The increase in GluR1 and GluR2/3, but no increase in GluR2 subunits suggests that there could be an increase in calcium permeability of AMPA receptors in limbic/striatal brain regions after maprotiline treatment. This could lead to increased synaptic activity or plasticity in the hippocampus and striatum, and may underlie the therapeutic effect of maprotline, and possibly, other antidepressant drugs. |
doi_str_mv | 10.1007/s00221-005-0228-2 |
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The present study was carried out to study the expression of AMPA receptor subunits in different brain regions of mice that had been chronically injected with maprotiline. The latter is a modified tricyclic antidepressant that functions as a noradrenaline uptake inhibitor. Daily intraperitoneal injection with 10 mg/kg maprotiline for 30 days resulted in significantly increased GluR1 and GluR2/3 subunit expression in the nucleus accumbens and dorsal striatum as detected by immunohistochemistry; and significantly increased GluR1 and GluR2/3 expression in the hippocampus, as demonstrated by Western blot analysis. No change, or a decrease in GluR2 expression was detected in all the brain regions by both immunohistochemistry and Western blots. The increase in GluR1 and GluR2/3, but no increase in GluR2 subunits suggests that there could be an increase in calcium permeability of AMPA receptors in limbic/striatal brain regions after maprotiline treatment. This could lead to increased synaptic activity or plasticity in the hippocampus and striatum, and may underlie the therapeutic effect of maprotline, and possibly, other antidepressant drugs.</description><identifier>ISSN: 0014-4819</identifier><identifier>EISSN: 1432-1106</identifier><identifier>DOI: 10.1007/s00221-005-0228-2</identifier><identifier>PMID: 16320045</identifier><identifier>CODEN: EXBRAP</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Acids ; Animals ; Antidepressants ; Antidepressive Agents - pharmacology ; Biochemistry and metabolism ; Biological and medical sciences ; Brain ; Brain - anatomy & histology ; Brain - drug effects ; Central nervous system ; Drugs ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Glutamic Acid - physiology ; Immunohistochemistry ; Maprotiline - pharmacology ; Mice ; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration ; Norepinephrine - physiology ; Protein Subunits - metabolism ; Receptors, AMPA - metabolism ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Experimental brain research, 2006-04, Vol.170 (4), p.448-456</ispartof><rights>2006 INIST-CNRS</rights><rights>Springer-Verlag 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-706465646b0a63f86aa9f665e35679f70b09a2de4c9036bc10fac900b611698e3</citedby><cites>FETCH-LOGICAL-c387t-706465646b0a63f86aa9f665e35679f70b09a2de4c9036bc10fac900b611698e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17713289$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16320045$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TAN, Chav-Hoon</creatorcontrib><creatorcontrib>XIN HE</creatorcontrib><creatorcontrib>JUN YANG</creatorcontrib><creatorcontrib>ONE, Wei-Yi</creatorcontrib><title>Changes in AMPA subunit expression in the mouse brain after chronic treatment with the antidepressant maprotiline : a link between noradrenergic and glutamatergic function?</title><title>Experimental brain research</title><addtitle>Exp Brain Res</addtitle><description>Potentiation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function has been proposed as being useful in the treatment of depression, but thus far, little is known about the possible changes in AMPA receptor expression in the brain, after antidepressant treatment. The present study was carried out to study the expression of AMPA receptor subunits in different brain regions of mice that had been chronically injected with maprotiline. The latter is a modified tricyclic antidepressant that functions as a noradrenaline uptake inhibitor. Daily intraperitoneal injection with 10 mg/kg maprotiline for 30 days resulted in significantly increased GluR1 and GluR2/3 subunit expression in the nucleus accumbens and dorsal striatum as detected by immunohistochemistry; and significantly increased GluR1 and GluR2/3 expression in the hippocampus, as demonstrated by Western blot analysis. No change, or a decrease in GluR2 expression was detected in all the brain regions by both immunohistochemistry and Western blots. The increase in GluR1 and GluR2/3, but no increase in GluR2 subunits suggests that there could be an increase in calcium permeability of AMPA receptors in limbic/striatal brain regions after maprotiline treatment. This could lead to increased synaptic activity or plasticity in the hippocampus and striatum, and may underlie the therapeutic effect of maprotline, and possibly, other antidepressant drugs.</description><subject>Acids</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - anatomy & histology</subject><subject>Brain - drug effects</subject><subject>Central nervous system</subject><subject>Drugs</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glutamic Acid - physiology</subject><subject>Immunohistochemistry</subject><subject>Maprotiline - pharmacology</subject><subject>Mice</subject><subject>Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration</subject><subject>Norepinephrine - physiology</subject><subject>Protein Subunits - metabolism</subject><subject>Receptors, AMPA - metabolism</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0014-4819</issn><issn>1432-1106</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc-O0zAQxi0EYsvCA3BBFhLcAmM7sRMuqKr4Jy2CA5ytiTtpvSROsR0tvBMPibuttBIXDpa_sX_zaeyPsacCXgkA8zoBSCkqgKYqoq3kPbYStZKVEKDvsxWAqKu6Fd0Fe5TS9bFUBh6yC6GVBKibFfuz2WPYUeI-8PXnr2ueln4JPnP6dYiUkp_D8SrviU_zkoj3EUuNQ6bI3T7OwTueI2GeKGR-4_P-FsaQ_ZZuLYrkEx7inP3oA_E3HHkRP3hP-YYo8DBH3EYKFHfFDMOW78Yl44T5dDIsweUyyNvH7MGAY6In5_2SfX__7tvmY3X15cOnzfqqcqo1uTKga92U1QNqNbQasRu0bkg12nSDgR46lFuqXQdK907AgEVCr4XQXUvqkr08-Zahfy6Usp18cjSOGKh8gtWmVW2nxX9BWSZRUJsCPv8HvJ6XGMojrBSNqKWsoUDiBLk4pxRpsIfoJ4y_rQB7DNyeArclcHsM3MrS8-xsvPQTbe86zgkX4MUZwORwHCIG59MdZ4xQsu3UXzg2tP4</recordid><startdate>20060401</startdate><enddate>20060401</enddate><creator>TAN, Chav-Hoon</creator><creator>XIN HE</creator><creator>JUN YANG</creator><creator>ONE, Wei-Yi</creator><general>Springer</general><general>Springer Nature B.V</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>0-V</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88J</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2R</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060401</creationdate><title>Changes in AMPA subunit expression in the mouse brain after chronic treatment with the antidepressant maprotiline : a link between noradrenergic and glutamatergic function?</title><author>TAN, Chav-Hoon ; XIN HE ; JUN YANG ; ONE, Wei-Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-706465646b0a63f86aa9f665e35679f70b09a2de4c9036bc10fac900b611698e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acids</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Antidepressive Agents - pharmacology</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - anatomy & histology</topic><topic>Brain - drug effects</topic><topic>Central nervous system</topic><topic>Drugs</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glutamic Acid - physiology</topic><topic>Immunohistochemistry</topic><topic>Maprotiline - pharmacology</topic><topic>Mice</topic><topic>Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration</topic><topic>Norepinephrine - physiology</topic><topic>Protein Subunits - metabolism</topic><topic>Receptors, AMPA - metabolism</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TAN, Chav-Hoon</creatorcontrib><creatorcontrib>XIN HE</creatorcontrib><creatorcontrib>JUN YANG</creatorcontrib><creatorcontrib>ONE, Wei-Yi</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>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Social Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>TAN, Chav-Hoon</au><au>XIN HE</au><au>JUN YANG</au><au>ONE, Wei-Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in AMPA subunit expression in the mouse brain after chronic treatment with the antidepressant maprotiline : a link between noradrenergic and glutamatergic function?</atitle><jtitle>Experimental brain research</jtitle><addtitle>Exp Brain Res</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>170</volume><issue>4</issue><spage>448</spage><epage>456</epage><pages>448-456</pages><issn>0014-4819</issn><eissn>1432-1106</eissn><coden>EXBRAP</coden><abstract>Potentiation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function has been proposed as being useful in the treatment of depression, but thus far, little is known about the possible changes in AMPA receptor expression in the brain, after antidepressant treatment. The present study was carried out to study the expression of AMPA receptor subunits in different brain regions of mice that had been chronically injected with maprotiline. The latter is a modified tricyclic antidepressant that functions as a noradrenaline uptake inhibitor. Daily intraperitoneal injection with 10 mg/kg maprotiline for 30 days resulted in significantly increased GluR1 and GluR2/3 subunit expression in the nucleus accumbens and dorsal striatum as detected by immunohistochemistry; and significantly increased GluR1 and GluR2/3 expression in the hippocampus, as demonstrated by Western blot analysis. No change, or a decrease in GluR2 expression was detected in all the brain regions by both immunohistochemistry and Western blots. The increase in GluR1 and GluR2/3, but no increase in GluR2 subunits suggests that there could be an increase in calcium permeability of AMPA receptors in limbic/striatal brain regions after maprotiline treatment. This could lead to increased synaptic activity or plasticity in the hippocampus and striatum, and may underlie the therapeutic effect of maprotline, and possibly, other antidepressant drugs.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>16320045</pmid><doi>10.1007/s00221-005-0228-2</doi><tpages>9</tpages></addata></record> |
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subjects | Acids Animals Antidepressants Antidepressive Agents - pharmacology Biochemistry and metabolism Biological and medical sciences Brain Brain - anatomy & histology Brain - drug effects Central nervous system Drugs Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Glutamic Acid - physiology Immunohistochemistry Maprotiline - pharmacology Mice Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration Norepinephrine - physiology Protein Subunits - metabolism Receptors, AMPA - metabolism Time Factors Vertebrates: nervous system and sense organs |
title | Changes in AMPA subunit expression in the mouse brain after chronic treatment with the antidepressant maprotiline : a link between noradrenergic and glutamatergic function? |
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