Modulation of inhibitory control networks relate to clinical response following ketamine therapy in major depression
Subanesthetic ketamine is found to induce fast-acting and pronounced antidepressant effects, even in treatment resistant depression (TRD). However, it remains unclear how ketamine modulates neural function at the brain systems-level to regulate emotion and behavior. Here, we examined treatment-relat...
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| Veröffentlicht in: | Translational psychiatry 2020-07, Vol.10 (1), p.260-260, Article 260 |
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| creator | Sahib, Ashish K. Loureiro, Joana RA Vasavada, Megha M. Kubicki, Antoni Wade, Benjamin Joshi, Shantanu H. Woods, Roger P. Congdon, Eliza Espinoza, Randall Narr, Katherine L. |
| description | Subanesthetic ketamine is found to induce fast-acting and pronounced antidepressant effects, even in treatment resistant depression (TRD). However, it remains unclear how ketamine modulates neural function at the brain systems-level to regulate emotion and behavior. Here, we examined treatment-related changes in the inhibitory control network after single and repeated ketamine therapy in TRD. Forty-seven TRD patients (mean age = 38, 19 women) and 32 healthy controls (mean age = 35, 18 women) performed a functional magnetic resonance imaging (fMRI) response inhibition task at baseline, and 37 patients completed the fMRI task and symptom scales again 24 h after receiving both one and four 0.5 mg/kg intravenous ketamine infusions. Analyses of fMRI data addressed effects of diagnosis, time, and differences between treatment remitters and non-remitters. Significant decreases in brain activation were observed in the inhibitory control network, including in prefrontal and parietal regions, and visual cortex following serial ketamine treatment,
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| doi_str_mv | 10.1038/s41398-020-00947-7 |
| format | Article |
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p
< 0.05 corrected. Remitters were distinguished from non-remitters by having lower functional activation in the supplementary motor area (SMA) prior to treatment, which normalized towards controls following serial ketamine treatment. Results suggest that ketamine treatment leads to neurofunctional plasticity in executive control networks including the SMA during a response-inhibitory task. SMA changes relate to reductions in depressive symptoms, suggesting modulation of this network play an important role in therapeutic response. In addition, early changes in the SMA network during response inhibition appear predictive of overall treatment outcome, and may serve as a biomarker of treatment response.</description><identifier>ISSN: 2158-3188</identifier><identifier>EISSN: 2158-3188</identifier><identifier>DOI: 10.1038/s41398-020-00947-7</identifier><identifier>PMID: 32732915</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/154/53/2423 ; 692/53/2421 ; Adult ; Antidepressive Agents - therapeutic use ; Behavioral Sciences ; Biological Psychology ; Depression ; Depressive Disorder, Major - drug therapy ; Depressive Disorder, Treatment-Resistant - diagnostic imaging ; Depressive Disorder, Treatment-Resistant - drug therapy ; Female ; Humans ; Ketamine ; Ketamine - therapeutic use ; Medicine ; Medicine & Public Health ; Neurosciences ; Pharmacotherapy ; Psychiatry</subject><ispartof>Translational psychiatry, 2020-07, Vol.10 (1), p.260-260, Article 260</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-beca2d4dbf8407f690361f39c731198b9264c770cb4ec26fd62a7706e0806b6b3</citedby><cites>FETCH-LOGICAL-c502t-beca2d4dbf8407f690361f39c731198b9264c770cb4ec26fd62a7706e0806b6b3</cites><orcidid>0000-0003-0622-9634 ; 0000-0003-2895-4212</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393172/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7393172/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32732915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sahib, Ashish K.</creatorcontrib><creatorcontrib>Loureiro, Joana RA</creatorcontrib><creatorcontrib>Vasavada, Megha M.</creatorcontrib><creatorcontrib>Kubicki, Antoni</creatorcontrib><creatorcontrib>Wade, Benjamin</creatorcontrib><creatorcontrib>Joshi, Shantanu H.</creatorcontrib><creatorcontrib>Woods, Roger P.</creatorcontrib><creatorcontrib>Congdon, Eliza</creatorcontrib><creatorcontrib>Espinoza, Randall</creatorcontrib><creatorcontrib>Narr, Katherine L.</creatorcontrib><title>Modulation of inhibitory control networks relate to clinical response following ketamine therapy in major depression</title><title>Translational psychiatry</title><addtitle>Transl Psychiatry</addtitle><addtitle>Transl Psychiatry</addtitle><description>Subanesthetic ketamine is found to induce fast-acting and pronounced antidepressant effects, even in treatment resistant depression (TRD). However, it remains unclear how ketamine modulates neural function at the brain systems-level to regulate emotion and behavior. Here, we examined treatment-related changes in the inhibitory control network after single and repeated ketamine therapy in TRD. Forty-seven TRD patients (mean age = 38, 19 women) and 32 healthy controls (mean age = 35, 18 women) performed a functional magnetic resonance imaging (fMRI) response inhibition task at baseline, and 37 patients completed the fMRI task and symptom scales again 24 h after receiving both one and four 0.5 mg/kg intravenous ketamine infusions. Analyses of fMRI data addressed effects of diagnosis, time, and differences between treatment remitters and non-remitters. Significant decreases in brain activation were observed in the inhibitory control network, including in prefrontal and parietal regions, and visual cortex following serial ketamine treatment,
p
< 0.05 corrected. Remitters were distinguished from non-remitters by having lower functional activation in the supplementary motor area (SMA) prior to treatment, which normalized towards controls following serial ketamine treatment. Results suggest that ketamine treatment leads to neurofunctional plasticity in executive control networks including the SMA during a response-inhibitory task. SMA changes relate to reductions in depressive symptoms, suggesting modulation of this network play an important role in therapeutic response. In addition, early changes in the SMA network during response inhibition appear predictive of overall treatment outcome, and may serve as a biomarker of treatment response.</description><subject>631/154/53/2423</subject><subject>692/53/2421</subject><subject>Adult</subject><subject>Antidepressive Agents - therapeutic use</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Depression</subject><subject>Depressive Disorder, Major - drug therapy</subject><subject>Depressive Disorder, Treatment-Resistant - diagnostic imaging</subject><subject>Depressive Disorder, Treatment-Resistant - drug therapy</subject><subject>Female</subject><subject>Humans</subject><subject>Ketamine</subject><subject>Ketamine - therapeutic use</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurosciences</subject><subject>Pharmacotherapy</subject><subject>Psychiatry</subject><issn>2158-3188</issn><issn>2158-3188</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9kUtv1DAUhS0EotXQP8ACWWLDJuBH4scGCVVAkYrYwNpyHGfGU8cOdtJq_j2XTimFRb3x434-9x4dhF5S8pYSrt7VlnKtGsJIQ4huZSOfoFNGO9VwqtTTB-cTdFbrnsDqWkUlfY5OOJOcadqdouVrHtZol5ATziMOaRf6sORywC6npeSIk19ucrmquHjgPF4ydjGk4GyEpzrnVD0ec4z5JqQtvvKLnUICbueLnQ8giSe7zwUPfga-QqcX6NloY_Vnd_sG_fj08fv5RXP57fOX8w-XjesIW5reO8uGduhH1RI5Ck24oCPXTnJKteo1E62Tkri-9Y6JcRDMwlV4oojoRc836P1Rd177yQ_OgyMbzVzCZMvBZBvMv5UUdmabr43kmlPJQODNnUDJP1dfFzOF6nyMNvm8VsNapqUUShFAX_-H7vNaEtgDSknWKaK7xymmpABPFCh2pFzJtRY_3o9MifmdvjmmbyB9c5s-TLxBrx6avf_yJ2sA-BGoUEpbX_72fkT2F3hPvMk</recordid><startdate>20200730</startdate><enddate>20200730</enddate><creator>Sahib, Ashish K.</creator><creator>Loureiro, Joana RA</creator><creator>Vasavada, Megha M.</creator><creator>Kubicki, Antoni</creator><creator>Wade, Benjamin</creator><creator>Joshi, Shantanu H.</creator><creator>Woods, Roger P.</creator><creator>Congdon, Eliza</creator><creator>Espinoza, Randall</creator><creator>Narr, Katherine L.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0622-9634</orcidid><orcidid>https://orcid.org/0000-0003-2895-4212</orcidid></search><sort><creationdate>20200730</creationdate><title>Modulation of inhibitory control networks relate to clinical response following ketamine therapy in major depression</title><author>Sahib, Ashish K. ; 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However, it remains unclear how ketamine modulates neural function at the brain systems-level to regulate emotion and behavior. Here, we examined treatment-related changes in the inhibitory control network after single and repeated ketamine therapy in TRD. Forty-seven TRD patients (mean age = 38, 19 women) and 32 healthy controls (mean age = 35, 18 women) performed a functional magnetic resonance imaging (fMRI) response inhibition task at baseline, and 37 patients completed the fMRI task and symptom scales again 24 h after receiving both one and four 0.5 mg/kg intravenous ketamine infusions. Analyses of fMRI data addressed effects of diagnosis, time, and differences between treatment remitters and non-remitters. Significant decreases in brain activation were observed in the inhibitory control network, including in prefrontal and parietal regions, and visual cortex following serial ketamine treatment,
p
< 0.05 corrected. Remitters were distinguished from non-remitters by having lower functional activation in the supplementary motor area (SMA) prior to treatment, which normalized towards controls following serial ketamine treatment. Results suggest that ketamine treatment leads to neurofunctional plasticity in executive control networks including the SMA during a response-inhibitory task. SMA changes relate to reductions in depressive symptoms, suggesting modulation of this network play an important role in therapeutic response. In addition, early changes in the SMA network during response inhibition appear predictive of overall treatment outcome, and may serve as a biomarker of treatment response.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32732915</pmid><doi>10.1038/s41398-020-00947-7</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-0622-9634</orcidid><orcidid>https://orcid.org/0000-0003-2895-4212</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/154/53/2423 692/53/2421 Adult Antidepressive Agents - therapeutic use Behavioral Sciences Biological Psychology Depression Depressive Disorder, Major - drug therapy Depressive Disorder, Treatment-Resistant - diagnostic imaging Depressive Disorder, Treatment-Resistant - drug therapy Female Humans Ketamine Ketamine - therapeutic use Medicine Medicine & Public Health Neurosciences Pharmacotherapy Psychiatry |
| title | Modulation of inhibitory control networks relate to clinical response following ketamine therapy in major depression |
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