{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:63240"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:63240","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Serotonergic modulation of response inhibition : a fMRI study","abstract":"In animal and human studies, the neurotransmitter serotonin (5-HT) has been implicated in inhibitory control. Using functional magnetic response imaging (fMRI), the present study investigated the acute effects of pharmacological modulation in the serotonergic system on brain activations during response inhibition in healthy human volunteers. In all, 14 male participants received either a single oral dose of selective serotonin reuptake inhibitor (SSRI) escitalopram (10 mg) or placebo in a randomized double-blind placebo-controlled cross-over design. At the time of the expected plasma peak participants performed a stop change task during fMRI. Functional images were analyzed using Statistical Parametric Mapping software (SPM5). Escitalopram did not affect behavioral inhibitory performance as the main effect did not reveal significant differences of stop signal reaction time (SSRT). Likewise no differences were found for reaction time on go-trials (goRT) as well as for reaction time on trials of unsuccessful response inhibition (StopRespondRT). However, escitalopram was associated with alterations in brain activation patterns compared to placebo. Escitalopram enhanced brain activations in right prefrontal cortex, including right OFC, in right supplementary/pre motor and bilateral cingulate cortex as well as in subcortical regions during successful response inhibition. Also, escitalopram modulated a widespread network of brain regions, including anterior cingulate, right parietal cortex, right OFC, areas in right temporal cortex and subcortical regions during failed inhibition. During the go-process escitalopram increased brain activations in numerous regions like right anterior and posterior cingulate and in right prefrontal, parietal and temporal cortex as well as in subcortical areas. Our findings implicate an involvement of 5-HT in neural regulation of response inhibition. Moreover, this study provides evidence that 5-HT influences not only action restraint but also action cancellation through modulation of activations of brain areas. In addition, we found modulating effects of serotonin also on activations during failed inhibition. Especially, the anterior cingulate seems to play a critical role here. Results of this study support the assumption of an involvement of the anterior cingulate in error-detection. The results also implicate a fronto-striatal-circuitry for response inhibition in conjunction with serotonin.","abstract_html":"In animal and human studies, the neurotransmitter serotonin (5-HT) has been implicated in inhibitory control. Using functional magnetic response imaging (fMRI), the present study investigated the acute effects of pharmacological modulation in the serotonergic system on brain activations during response inhibition in healthy human volunteers. In all, 14 male participants received either a single oral dose of selective serotonin reuptake inhibitor (SSRI) escitalopram (10 mg) or placebo in a randomized double-blind placebo-controlled cross-over design. At the time of the expected plasma peak participants performed a stop change task during fMRI. Functional images were analyzed using Statistical Parametric Mapping software (SPM5). Escitalopram did not affect behavioral inhibitory performance as the main effect did not reveal significant differences of stop signal reaction time (SSRT). Likewise no differences were found for reaction time on go-trials (goRT) as well as for reaction time on trials of unsuccessful response inhibition (StopRespondRT). However, escitalopram was associated with alterations in brain activation patterns compared to placebo. Escitalopram enhanced brain activations in right prefrontal cortex, including right OFC, in right supplementary/pre motor and bilateral cingulate cortex as well as in subcortical regions during successful response inhibition. Also, escitalopram modulated a widespread network of brain regions, including anterior cingulate, right parietal cortex, right OFC, areas in right temporal cortex and subcortical regions during failed inhibition. During the go-process escitalopram increased brain activations in numerous regions like right anterior and posterior cingulate and in right prefrontal, parietal and temporal cortex as well as in subcortical areas. Our findings implicate an involvement of 5-HT in neural regulation of response inhibition. Moreover, this study provides evidence that 5-HT influences not only action restraint but also action cancellation through modulation of activations of brain areas. In addition, we found modulating effects of serotonin also on activations during failed inhibition. Especially, the anterior cingulate seems to play a critical role here. Results of this study support the assumption of an involvement of the anterior cingulate in error-detection. 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However, escitalopram was associated with alterations in brain activation patterns compared to placebo. Escitalopram enhanced brain activations in right prefrontal cortex, including right OFC, in right supplementary/pre motor and bilateral cingulate cortex as well as in subcortical regions during successful response inhibition. Also, escitalopram modulated a widespread network of brain regions, including anterior cingulate, right parietal cortex, right OFC, areas in right temporal cortex and subcortical regions during failed inhibition. During the go-process escitalopram increased brain activations in numerous regions like right anterior and posterior cingulate and in right prefrontal, parietal and temporal cortex as well as in subcortical areas. Our findings implicate an involvement of 5-HT in neural regulation of response inhibition. Moreover, this study provides evidence that 5-HT influences not only action restraint but also action cancellation through modulation of activations of brain areas. In addition, we found modulating effects of serotonin also on activations during failed inhibition. Especially, the anterior cingulate seems to play a critical role here. Results of this study support the assumption of an involvement of the anterior cingulate in error-detection. The results also implicate a fronto-striatal-circuitry for response inhibition in conjunction with serotonin."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University III, 45 S. : Ill., graph. Darst. (2010). = Aachen, Techn. 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