Effect of variability of sequence length of go trials preceding a stop trial on ability of response inhibition in stop-signal task

2018 ◽  
Vol 35 (2) ◽  
pp. 95-102 ◽  
Author(s):  
Koichi Hiraoka ◽  
Atsushi Kinoshita ◽  
Hiroshi Kunimura ◽  
Masakazu Matsuoka
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mario Paci ◽  
Giulio Di Cosmo ◽  
Mauro Gianni Perrucci ◽  
Francesca Ferri ◽  
Marcello Costantini

AbstractInhibitory control is the ability to suppress inappropriate movements and unwanted actions, allowing to regulate impulses and responses. This ability can be measured via the Stop Signal Task, which provides a temporal index of response inhibition, namely the stop signal reaction time (SSRT). At the neural level, Transcranial Magnetic Stimulation (TMS) allows to investigate motor inhibition within the primary motor cortex (M1), such as the cortical silent period (CSP) which is an index of GABAB-mediated intracortical inhibition within M1. Although there is strong evidence that intracortical inhibition varies during action stopping, it is still not clear whether differences in the neurophysiological markers of intracortical inhibition contribute to behavioral differences in actual inhibitory capacities. Hence, here we explored the relationship between intracortical inhibition within M1 and behavioral response inhibition. GABABergic-mediated inhibition in M1 was determined by the duration of CSP, while behavioral inhibition was assessed by the SSRT. We found a significant positive correlation between CSP’s duration and SSRT, namely that individuals with greater levels of GABABergic-mediated inhibition seem to perform overall worse in inhibiting behavioral responses. These results support the assumption that individual differences in intracortical inhibition are mirrored by individual differences in action stopping abilities.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Charlotte L. Rae ◽  
Vanessa E. Botan ◽  
Cassandra D. Gould van Praag ◽  
Aleksandra M. Herman ◽  
Jasmina A. K. Nyyssönen ◽  
...  

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S63-S63
Author(s):  
Ya Wang ◽  
Lu-xia Jia ◽  
Xiao-jing Qin ◽  
Jun-yan Ye ◽  
Raymond Chan

Abstract Background Schizotypy, a subclinical group at risk for schizophrenia, have been found to show impairments in response inhibition. Recent studies differentiated proactive inhibition (a preparatory process before the stimuli appears) and reactive inhibition (the inhibition of a pre-potent or already initiated response). However, it remains unclear whether both proactive and reactive inhibition are impaired in schizotypy and what are the neural mechanisms. The present event-related potential study used an adapted stop-signal task to examine the two inhibition processes and the underlying neural mechanisms in schizotypy compared to healthy controls (HC). Methods A total of 21 individuals with schizotypy and 25 matched HC participated in this study. To explore different degrees of proactive inhibition, we set three conditions: a “certain” go condition which no stop signal occurred, a “17% no go” condition in which stop signal would appear in 17% of trials, and a “33% no go” condition in which stop signal would appear in 33% of trials. All participants completed all the conditions, and EEG was recorded when participants completed the task. Results Behavioral results showed that in both schizotypy and HC, the reaction times (RT) of go trials were significantly prolonged as the no go percentage increased, and HC showed significantly longer go RT compared with schizotypy in both “17% no go” and “33% no go” conditions, suggesting greater proactive inhibition in HC. Stop signal reaction times (SSRTs) in “33% no go” condition was shorter than “17% no go” condition in both groups. Schizotypy showed significantly longer SSRTs in both “17% no go” and “33% no go” conditions than HC, indicating schizotypy relied more on reactive inhibition. ERP results showed that schizotypy showed larger overall N1 for go trials than HC irrespective of condition, which may indicate a compensation process in schizotypy. Schizotypy showed smaller N2 on both successful and unsuccessful stop trials in “17% no go” conditions than HC, while no group difference was found in “33% no go” conditions for stop trials, which may indicate impaired error processing. Discussion These results suggested that schizotypy tended to be impaired in both proactive control and reactive control processes.


2020 ◽  
Vol 57 (10) ◽  
Author(s):  
P. Skippen ◽  
W. R. Fulham ◽  
P. T. Michie ◽  
D. Matzke ◽  
A. Heathcote ◽  
...  

2010 ◽  
Vol 206 (4) ◽  
pp. 351-358 ◽  
Author(s):  
Daniel J. Upton ◽  
Peter G. Enticott ◽  
Rodney J. Croft ◽  
Nicholas R. Cooper ◽  
Paul B. Fitzgerald

2009 ◽  
Vol 29 (50) ◽  
pp. 15870-15877 ◽  
Author(s):  
J. Chikazoe ◽  
K. Jimura ◽  
S. Hirose ◽  
K.-i. Yamashita ◽  
Y. Miyashita ◽  
...  

NeuroImage ◽  
2008 ◽  
Vol 41 (4) ◽  
pp. 1352-1363 ◽  
Author(s):  
Chiang-Shan Ray Li ◽  
Peisi Yan ◽  
Rajita Sinha ◽  
Tien-Wen Lee

2020 ◽  
Author(s):  
Claire O'Callaghan ◽  
Frank Hubert Hezemans ◽  
Rong Ye ◽  
Catarina Rua ◽  
P Simon Jones ◽  
...  

Cognitive decline is a common feature of Parkinson's disease, and many of these cognitive deficits fail to respond to dopaminergic therapy. Therefore, targeting other neuromodulatory systems represents an important therapeutic strategy. Among these, the locus coeruleus-noradrenaline system has been extensively implicated in response inhibition deficits. Restoring noradrenaline levels using the noradrenergic reuptake inhibitor atomoxetine can improve response inhibition in some patients with Parkinson's disease, but there is considerable heterogeneity in treatment response. Accurately predicting the patients who would benefit from therapies targeting this neurotransmitter system remains a critical goal, in order to design the necessary clinical trials with stratified patient selection to establish the therapeutic potential of atomoxetine. Here, we test the hypothesis that integrity of the noradrenergic locus coeruleus explains the variation in improvement of response inhibition following atomoxetine. In a double-blind placebo-controlled randomised crossover design, 19 people with Parkinson's disease completed an acute psychopharmacological challenge with 40 mg of oral atomoxetine or placebo. A stop-signal task was used to measure response inhibition, with stop-signal reaction times obtained through hierarchical Bayesian estimation of an ex-Gaussian race model. Twenty-six control subjects completed the same task without undergoing the drug manipulation. In a separate session, patients and controls underwent ultra-high field 7T imaging of the locus coeruleus using a neuromelanin-sensitive magnetisation transfer sequence. The principal result was that atomoxetine improved stop-signal reaction times in those patients with lower locus coeruleus integrity. This was in the context of a general impairment in response inhibition, as patients on placebo had longer stop-signal reaction times compared to controls. We also found that the caudal portion of the locus coeruleus showed the largest neuromelanin signal decrease in the patients compared to controls. Our results highlight a link between the integrity of the noradrenergic locus coeruleus and response inhibition in Parkinson's disease patients. Furthermore, they demonstrate the importance of baseline noradrenergic state in determining the response to atomoxetine. We suggest that locus coeruleus neuromelanin imaging offers a marker of noradrenergic capacity that could be used to stratify patients in trials of noradrenergic therapy and to ultimately inform personalised treatment approaches.


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