Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression
Proton magnetic resonance spectroscopy ( 1 HMRS) is an in vivo brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline 1 HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open tr...
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| Veröffentlicht in: | Neuropsychopharmacology (New York, N.Y.) N.Y.), 2007-12, Vol.32 (12), p.2490-2499 |
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| creator | Frye, Mark A Watzl, June Banakar, Shida O'Neill, Joseph Mintz, Jim Davanzo, Pablo Fischer, Jeffrey Chirichigno, Jason W Ventura, Joseph Elman, Shana Tsuang, John Walot, Irwin Thomas, M Albert |
| description | Proton magnetic resonance spectroscopy (
1
HMRS) is an
in vivo
brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline
1
HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open trial of lamotrigine, an anti-glutamatergic mood stabilizer. Twenty-three bipolar depressed and 12 control subjects underwent a MRS scan of the anterior cingulate/medial prefrontal cortex. The scan was performed on a GE whole-body 1.5 T MRI scanner using single-voxel PRESS (TE/TR=30/3000 ms, 3 × 3 × 3 cm
3
and post-processed offline with LCModel. Baseline CSF-corrected absolute concentrations of glutamate+glutamine ([Glx]), glutamate ([Glu]), and creatine+phosphocreatine ([Cr]) were significantly higher in bipolar depressed subjects
vs
healthy controls. The non-melancholic subtype had significantly higher baseline [Glx] and [Glu] levels than the melancholic subtype. Remission with lamotrigine was associated with significantly lower post-treatment glutamine ([Gln]) in comparison to non-remission. These data suggest that non-melancholic bipolar depression is characterized by increased glutamate coupled with increased energy expenditure. Lamotrigine appears to reduce glutamine levels associated with treatment remission. Further study is encouraged to determine if these MR spectroscopic markers can delineate drug mechanism of action and subsequent treatment response. |
| doi_str_mv | 10.1038/sj.npp.1301387 |
| format | Article |
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1
HMRS) is an
in vivo
brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline
1
HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open trial of lamotrigine, an anti-glutamatergic mood stabilizer. Twenty-three bipolar depressed and 12 control subjects underwent a MRS scan of the anterior cingulate/medial prefrontal cortex. The scan was performed on a GE whole-body 1.5 T MRI scanner using single-voxel PRESS (TE/TR=30/3000 ms, 3 × 3 × 3 cm
3
and post-processed offline with LCModel. Baseline CSF-corrected absolute concentrations of glutamate+glutamine ([Glx]), glutamate ([Glu]), and creatine+phosphocreatine ([Cr]) were significantly higher in bipolar depressed subjects
vs
healthy controls. The non-melancholic subtype had significantly higher baseline [Glx] and [Glu] levels than the melancholic subtype. Remission with lamotrigine was associated with significantly lower post-treatment glutamine ([Gln]) in comparison to non-remission. These data suggest that non-melancholic bipolar depression is characterized by increased glutamate coupled with increased energy expenditure. Lamotrigine appears to reduce glutamine levels associated with treatment remission. Further study is encouraged to determine if these MR spectroscopic markers can delineate drug mechanism of action and subsequent treatment response.</description><identifier>ISSN: 0893-133X</identifier><identifier>EISSN: 1740-634X</identifier><identifier>DOI: 10.1038/sj.npp.1301387</identifier><identifier>PMID: 17429412</identifier><identifier>CODEN: NEROEW</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Adult ; Adult and adolescent clinical studies ; Analysis of Variance ; Antidepressive Agents - pharmacology ; Antidepressive Agents - therapeutic use ; Behavioral Sciences ; Biological and medical sciences ; Biological Psychology ; Bipolar disorder ; Bipolar Disorder - cerebrospinal fluid ; Bipolar Disorder - drug therapy ; Bipolar Disorder - metabolism ; Bipolar Disorder - pathology ; Bipolar disorders ; Creatine - metabolism ; Depression ; Evaluation Studies as Topic ; Female ; Glutamic Acid - metabolism ; Gyrus Cinguli - drug effects ; Gyrus Cinguli - metabolism ; Humans ; Magnetic Resonance Spectroscopy - methods ; Male ; Medical imaging ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Mood disorders ; Neurosciences ; original-article ; Pharmacotherapy ; Prefrontal Cortex - drug effects ; Prefrontal Cortex - metabolism ; Protons ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychotropic drugs ; Spectrum analysis ; Triazines - pharmacology ; Triazines - therapeutic use</subject><ispartof>Neuropsychopharmacology (New York, N.Y.), 2007-12, Vol.32 (12), p.2490-2499</ispartof><rights>American College of Neuropsychopharmacology 2007</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-91f63fba002c06693a6cc3f986372679d229cb0d771c22352e6d25258653f2a13</citedby><cites>FETCH-LOGICAL-c496t-91f63fba002c06693a6cc3f986372679d229cb0d771c22352e6d25258653f2a13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.npp.1301387$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.npp.1301387$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19560459$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17429412$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frye, Mark A</creatorcontrib><creatorcontrib>Watzl, June</creatorcontrib><creatorcontrib>Banakar, Shida</creatorcontrib><creatorcontrib>O'Neill, Joseph</creatorcontrib><creatorcontrib>Mintz, Jim</creatorcontrib><creatorcontrib>Davanzo, Pablo</creatorcontrib><creatorcontrib>Fischer, Jeffrey</creatorcontrib><creatorcontrib>Chirichigno, Jason W</creatorcontrib><creatorcontrib>Ventura, Joseph</creatorcontrib><creatorcontrib>Elman, Shana</creatorcontrib><creatorcontrib>Tsuang, John</creatorcontrib><creatorcontrib>Walot, Irwin</creatorcontrib><creatorcontrib>Thomas, M Albert</creatorcontrib><title>Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression</title><title>Neuropsychopharmacology (New York, N.Y.)</title><addtitle>Neuropsychopharmacol</addtitle><addtitle>Neuropsychopharmacology</addtitle><description>Proton magnetic resonance spectroscopy (
1
HMRS) is an
in vivo
brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline
1
HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open trial of lamotrigine, an anti-glutamatergic mood stabilizer. Twenty-three bipolar depressed and 12 control subjects underwent a MRS scan of the anterior cingulate/medial prefrontal cortex. The scan was performed on a GE whole-body 1.5 T MRI scanner using single-voxel PRESS (TE/TR=30/3000 ms, 3 × 3 × 3 cm
3
and post-processed offline with LCModel. Baseline CSF-corrected absolute concentrations of glutamate+glutamine ([Glx]), glutamate ([Glu]), and creatine+phosphocreatine ([Cr]) were significantly higher in bipolar depressed subjects
vs
healthy controls. The non-melancholic subtype had significantly higher baseline [Glx] and [Glu] levels than the melancholic subtype. Remission with lamotrigine was associated with significantly lower post-treatment glutamine ([Gln]) in comparison to non-remission. These data suggest that non-melancholic bipolar depression is characterized by increased glutamate coupled with increased energy expenditure. Lamotrigine appears to reduce glutamine levels associated with treatment remission. Further study is encouraged to determine if these MR spectroscopic markers can delineate drug mechanism of action and subsequent treatment response.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Analysis of Variance</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Antidepressive Agents - therapeutic use</subject><subject>Behavioral Sciences</subject><subject>Biological and medical sciences</subject><subject>Biological Psychology</subject><subject>Bipolar disorder</subject><subject>Bipolar Disorder - cerebrospinal fluid</subject><subject>Bipolar Disorder - drug therapy</subject><subject>Bipolar Disorder - metabolism</subject><subject>Bipolar Disorder - pathology</subject><subject>Bipolar disorders</subject><subject>Creatine - metabolism</subject><subject>Depression</subject><subject>Evaluation Studies as Topic</subject><subject>Female</subject><subject>Glutamic Acid - metabolism</subject><subject>Gyrus Cinguli - drug effects</subject><subject>Gyrus Cinguli - metabolism</subject><subject>Humans</subject><subject>Magnetic Resonance Spectroscopy - methods</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mood disorders</subject><subject>Neurosciences</subject><subject>original-article</subject><subject>Pharmacotherapy</subject><subject>Prefrontal Cortex - drug effects</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Protons</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychotropic drugs</subject><subject>Spectrum analysis</subject><subject>Triazines - pharmacology</subject><subject>Triazines - therapeutic use</subject><issn>0893-133X</issn><issn>1740-634X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp10M1LwzAYBvAgipvTq0cpgt665aNJm-OsOgcTPSjsFrI0HRldUpP24H9vZIWB4Ckv5JcnLw8A1whOESTFLOymtm2niEBEivwEjFGewZSRbH0KxrDgJEWErEfgIoQdhIjmrDgHo4gwzxAeg2ppldcy6CqZ205743xSGrvtG9np2auujGySd69r72wXx9L5zqg4LJq-k_uIEmmrpIwZnbE6MTZ5MK1rpE8edet1CMbZS3BWyyboq-GcgM_np4_yJV29LZblfJWqjLMu5ahmpN5ICLGCjHEimVKk5gUjOWY5rzDmagOrPEcKY0KxZhWmmBaMkhpLRCbg_pDbevfV69CJvQlKN4202vVBsIJixCGN8PYP3Lne27ibwDGRZIgVEU0PSHkXQqxAtN7spf8WCIrf8kXYiVi-GMqPD26G1H6z19WRD21HcDcAGWKHtZdWmXB0nDKYUR7d7OBCvLJb7Y_r_fP1D64snMw</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Frye, Mark A</creator><creator>Watzl, June</creator><creator>Banakar, Shida</creator><creator>O'Neill, Joseph</creator><creator>Mintz, Jim</creator><creator>Davanzo, Pablo</creator><creator>Fischer, Jeffrey</creator><creator>Chirichigno, Jason W</creator><creator>Ventura, Joseph</creator><creator>Elman, Shana</creator><creator>Tsuang, John</creator><creator>Walot, Irwin</creator><creator>Thomas, M Albert</creator><general>Springer International Publishing</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20071201</creationdate><title>Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression</title><author>Frye, Mark A ; Watzl, June ; Banakar, Shida ; O'Neill, Joseph ; Mintz, Jim ; Davanzo, Pablo ; Fischer, Jeffrey ; Chirichigno, Jason W ; Ventura, Joseph ; Elman, Shana ; Tsuang, John ; Walot, Irwin ; Thomas, M Albert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-91f63fba002c06693a6cc3f986372679d229cb0d771c22352e6d25258653f2a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Analysis of Variance</topic><topic>Antidepressive Agents - pharmacology</topic><topic>Antidepressive Agents - therapeutic use</topic><topic>Behavioral Sciences</topic><topic>Biological and medical sciences</topic><topic>Biological Psychology</topic><topic>Bipolar disorder</topic><topic>Bipolar Disorder - cerebrospinal fluid</topic><topic>Bipolar Disorder - drug therapy</topic><topic>Bipolar Disorder - metabolism</topic><topic>Bipolar Disorder - pathology</topic><topic>Bipolar disorders</topic><topic>Creatine - metabolism</topic><topic>Depression</topic><topic>Evaluation Studies as Topic</topic><topic>Female</topic><topic>Glutamic Acid - metabolism</topic><topic>Gyrus Cinguli - drug effects</topic><topic>Gyrus Cinguli - metabolism</topic><topic>Humans</topic><topic>Magnetic Resonance Spectroscopy - methods</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mood disorders</topic><topic>Neurosciences</topic><topic>original-article</topic><topic>Pharmacotherapy</topic><topic>Prefrontal Cortex - drug effects</topic><topic>Prefrontal Cortex - metabolism</topic><topic>Protons</topic><topic>Psychiatry</topic><topic>Psychology. 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1
HMRS) is an
in vivo
brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline
1
HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open trial of lamotrigine, an anti-glutamatergic mood stabilizer. Twenty-three bipolar depressed and 12 control subjects underwent a MRS scan of the anterior cingulate/medial prefrontal cortex. The scan was performed on a GE whole-body 1.5 T MRI scanner using single-voxel PRESS (TE/TR=30/3000 ms, 3 × 3 × 3 cm
3
and post-processed offline with LCModel. Baseline CSF-corrected absolute concentrations of glutamate+glutamine ([Glx]), glutamate ([Glu]), and creatine+phosphocreatine ([Cr]) were significantly higher in bipolar depressed subjects
vs
healthy controls. The non-melancholic subtype had significantly higher baseline [Glx] and [Glu] levels than the melancholic subtype. Remission with lamotrigine was associated with significantly lower post-treatment glutamine ([Gln]) in comparison to non-remission. These data suggest that non-melancholic bipolar depression is characterized by increased glutamate coupled with increased energy expenditure. Lamotrigine appears to reduce glutamine levels associated with treatment remission. Further study is encouraged to determine if these MR spectroscopic markers can delineate drug mechanism of action and subsequent treatment response.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>17429412</pmid><doi>10.1038/sj.npp.1301387</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuropsychopharmacology (New York, N.Y.), 2007-12, Vol.32 (12), p.2490-2499 |
| issn | 0893-133X 1740-634X |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Adult Adult and adolescent clinical studies Analysis of Variance Antidepressive Agents - pharmacology Antidepressive Agents - therapeutic use Behavioral Sciences Biological and medical sciences Biological Psychology Bipolar disorder Bipolar Disorder - cerebrospinal fluid Bipolar Disorder - drug therapy Bipolar Disorder - metabolism Bipolar Disorder - pathology Bipolar disorders Creatine - metabolism Depression Evaluation Studies as Topic Female Glutamic Acid - metabolism Gyrus Cinguli - drug effects Gyrus Cinguli - metabolism Humans Magnetic Resonance Spectroscopy - methods Male Medical imaging Medical sciences Medicine Medicine & Public Health Middle Aged Mood disorders Neurosciences original-article Pharmacotherapy Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Protons Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychotropic drugs Spectrum analysis Triazines - pharmacology Triazines - therapeutic use |
| title | Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression |
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