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Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex

BACKGROUND: Patients on the selective serotonergic reuptake inhibitors like citalopram report emotional blunting. We showed previously that citalopram reduces resting-state functional connectivity in healthy volunteers in a number of brain regions, including the dorso-medial prefrontal cortex, which...

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Autores principales: Rzepa, Ewelina, Dean, Zola, McCabe, Ciara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458340/
https://www.ncbi.nlm.nih.gov/pubmed/28340244
http://dx.doi.org/10.1093/ijnp/pyx016
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author Rzepa, Ewelina
Dean, Zola
McCabe, Ciara
author_facet Rzepa, Ewelina
Dean, Zola
McCabe, Ciara
author_sort Rzepa, Ewelina
collection PubMed
description BACKGROUND: Patients on the selective serotonergic reuptake inhibitors like citalopram report emotional blunting. We showed previously that citalopram reduces resting-state functional connectivity in healthy volunteers in a number of brain regions, including the dorso-medial prefrontal cortex, which may be related to its clinical effects. Bupropion is a dopaminergic and noradrenergic reuptake inhibitor and is not reported to cause emotional blunting. However, how bupropion affects resting-state functional connectivity in healthy controls remains unknown. METHODS: Using a within-subjects, repeated-measures, double-blind, crossover design, we examined 17 healthy volunteers (9 female, 8 male). Volunteers received 7 days of bupropion (150 mg/d) and 7 days of placebo treatment and underwent resting-state functional Magnetic Resonance Imaging. We selected seed regions in the salience network (amygdala and pregenual anterior cingulate cortex) and the central executive network (dorsal medial prefrontal cortex). Mood and anhedonia measures were also recorded and examined in relation to resting-state functional connectivity. RESULTS: Relative to placebo, bupropion increased resting-state functional connectivity in healthy volunteers between the dorsal medial prefrontal cortex seed region and the posterior cingulate cortex and the precuneus cortex, key parts of the default mode network. CONCLUSIONS: These results are opposite to that which we found with 7 days treatment of citalopram in healthy volunteers. These results reflect a different mechanism of action of bupropion compared with selective serotonergic reuptake inhibitors. These results help explain the apparent lack of emotional blunting caused by bupropion in depressed patients.
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spelling pubmed-54583402017-06-08 Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex Rzepa, Ewelina Dean, Zola McCabe, Ciara Int J Neuropsychopharmacol Regular Research Article BACKGROUND: Patients on the selective serotonergic reuptake inhibitors like citalopram report emotional blunting. We showed previously that citalopram reduces resting-state functional connectivity in healthy volunteers in a number of brain regions, including the dorso-medial prefrontal cortex, which may be related to its clinical effects. Bupropion is a dopaminergic and noradrenergic reuptake inhibitor and is not reported to cause emotional blunting. However, how bupropion affects resting-state functional connectivity in healthy controls remains unknown. METHODS: Using a within-subjects, repeated-measures, double-blind, crossover design, we examined 17 healthy volunteers (9 female, 8 male). Volunteers received 7 days of bupropion (150 mg/d) and 7 days of placebo treatment and underwent resting-state functional Magnetic Resonance Imaging. We selected seed regions in the salience network (amygdala and pregenual anterior cingulate cortex) and the central executive network (dorsal medial prefrontal cortex). Mood and anhedonia measures were also recorded and examined in relation to resting-state functional connectivity. RESULTS: Relative to placebo, bupropion increased resting-state functional connectivity in healthy volunteers between the dorsal medial prefrontal cortex seed region and the posterior cingulate cortex and the precuneus cortex, key parts of the default mode network. CONCLUSIONS: These results are opposite to that which we found with 7 days treatment of citalopram in healthy volunteers. These results reflect a different mechanism of action of bupropion compared with selective serotonergic reuptake inhibitors. These results help explain the apparent lack of emotional blunting caused by bupropion in depressed patients. Oxford University Press 2017-03-11 /pmc/articles/PMC5458340/ /pubmed/28340244 http://dx.doi.org/10.1093/ijnp/pyx016 Text en © The Author 2017. Published by Oxford University Press on behalf of CINP. http://creativecommons.org/licenses/by/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Regular Research Article
Rzepa, Ewelina
Dean, Zola
McCabe, Ciara
Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title_full Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title_fullStr Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title_full_unstemmed Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title_short Bupropion Administration Increases Resting-State Functional Connectivity in Dorso-Medial Prefrontal Cortex
title_sort bupropion administration increases resting-state functional connectivity in dorso-medial prefrontal cortex
topic Regular Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5458340/
https://www.ncbi.nlm.nih.gov/pubmed/28340244
http://dx.doi.org/10.1093/ijnp/pyx016
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