Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans
Background: Studies in animals and humans have shown that cortical neuroplasticity can be modulated by increasing serotonin levels by administering selective serotonin reuptake inhibitors (SSRI). However, little is known about the mechanistic background, especially the contribution of intracortical...
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Elsevier
2024-03-01
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Series: | Brain Stimulation |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S1935861X24000597 |
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author | Lorena Melo Marie C. Beaupain Elham Ghanavati Min-Fang Kuo Michael A. Nitsche |
author_facet | Lorena Melo Marie C. Beaupain Elham Ghanavati Min-Fang Kuo Michael A. Nitsche |
author_sort | Lorena Melo |
collection | DOAJ |
description | Background: Studies in animals and humans have shown that cortical neuroplasticity can be modulated by increasing serotonin levels by administering selective serotonin reuptake inhibitors (SSRI). However, little is known about the mechanistic background, especially the contribution of intracortical inhibition and facilitation, which depend on gamma-aminobutyric acid (GABA) and glutamate. Objective: We aimed to explore the relevance of drivers of plasticity (glutamate- and GABA-dependent processes) for the effects of serotonin enhancement on tDCS-induced plasticity in healthy humans. Methods: A crossover, partially double-blinded, randomized, and sham-controlled study was conducted in 16 healthy right-handed individuals. In each of the 7 sessions, plasticity was induced via transcranial direct current stimulation (tDCS). Anodal, cathodal, and sham tDCS were applied to the left motor cortex under SSRI (20 mg/40 mg citalopram) or placebo. Short-interval cortical inhibition (SICI) and intracortical facilitation (ICF) were monitored by paired-pulse transcranial magnetic stimulation for 5–6 h after intervention. Results: Under placebo, anodal tDCS-induced LTP-like plasticity decreased SICI and increased ICF. In contrast, cathodal tDCS-elicited LTD-like plasticity induced the opposite effect. Under 20 mg and 40 mg citalopram, anodal tDCS did not affect SICI largely, while ICF was enhanced and prolonged. For cathodal tDCS, citalopram converted the increase of SICI and decrease of ICF into antagonistic effects, and this effect was dosage-dependent since it lasted longer under 40 mg when compared to 20 mg. Conclusion: We speculate that the main effects of acute serotonergic enhancement on tDCS-induced plasticity, the increase and prolongation of LTP-like plasticity effects, involves mainly the glutamatergic system. |
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institution | Directory Open Access Journal |
issn | 1935-861X |
language | English |
last_indexed | 2024-04-24T13:12:19Z |
publishDate | 2024-03-01 |
publisher | Elsevier |
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series | Brain Stimulation |
spelling | doaj.art-f8c0deb9d54c4b598c5154eed838c5a72024-04-05T04:40:12ZengElsevierBrain Stimulation1935-861X2024-03-01172421430Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humansLorena Melo0Marie C. Beaupain1Elham Ghanavati2Min-Fang Kuo3Michael A. Nitsche4Department of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, GermanyDepartment of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, Germany; Department of Psychology, Ruhr-University Bochum, GermanyDepartment of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, Germany; Department of Psychology, Ruhr-University Bochum, GermanyDepartment of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, Germany; Corresponding author. Dept. Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Ardeystraße 67, 44139 Dortmund, Germany.Department of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, Germany; Bielefeld University, University Hospital OWL, Protestant Hospital of Bethel Foundation, University Clinic of Psychiatry and Psychotherapy and University Clinic of Child and Adolescent Psychiatry and Psychotherapy, Germany; German Center for Mental Health (DZPG), Partner Site - Bochum/Marburg, GermanyBackground: Studies in animals and humans have shown that cortical neuroplasticity can be modulated by increasing serotonin levels by administering selective serotonin reuptake inhibitors (SSRI). However, little is known about the mechanistic background, especially the contribution of intracortical inhibition and facilitation, which depend on gamma-aminobutyric acid (GABA) and glutamate. Objective: We aimed to explore the relevance of drivers of plasticity (glutamate- and GABA-dependent processes) for the effects of serotonin enhancement on tDCS-induced plasticity in healthy humans. Methods: A crossover, partially double-blinded, randomized, and sham-controlled study was conducted in 16 healthy right-handed individuals. In each of the 7 sessions, plasticity was induced via transcranial direct current stimulation (tDCS). Anodal, cathodal, and sham tDCS were applied to the left motor cortex under SSRI (20 mg/40 mg citalopram) or placebo. Short-interval cortical inhibition (SICI) and intracortical facilitation (ICF) were monitored by paired-pulse transcranial magnetic stimulation for 5–6 h after intervention. Results: Under placebo, anodal tDCS-induced LTP-like plasticity decreased SICI and increased ICF. In contrast, cathodal tDCS-elicited LTD-like plasticity induced the opposite effect. Under 20 mg and 40 mg citalopram, anodal tDCS did not affect SICI largely, while ICF was enhanced and prolonged. For cathodal tDCS, citalopram converted the increase of SICI and decrease of ICF into antagonistic effects, and this effect was dosage-dependent since it lasted longer under 40 mg when compared to 20 mg. Conclusion: We speculate that the main effects of acute serotonergic enhancement on tDCS-induced plasticity, the increase and prolongation of LTP-like plasticity effects, involves mainly the glutamatergic system.http://www.sciencedirect.com/science/article/pii/S1935861X24000597SerotoninNeuroplasticityTranscranial direct current stimulationTranscranial magnetic stimulation |
spellingShingle | Lorena Melo Marie C. Beaupain Elham Ghanavati Min-Fang Kuo Michael A. Nitsche Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans Brain Stimulation Serotonin Neuroplasticity Transcranial direct current stimulation Transcranial magnetic stimulation |
title | Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
title_full | Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
title_fullStr | Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
title_full_unstemmed | Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
title_short | Neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
title_sort | neurochemical mechanisms underlying serotonergic modulation of neuroplasticity in humans |
topic | Serotonin Neuroplasticity Transcranial direct current stimulation Transcranial magnetic stimulation |
url | http://www.sciencedirect.com/science/article/pii/S1935861X24000597 |
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