A year in research · 30 selected publications · five research threads
Our 2019 studies showed that response inhibition cannot be understood without the perceptual, learned and biological context in which stopping becomes necessary.
The year dismantled the idea of a single inhibitory mechanism. Conflict source, stimulus modality, expectation, prior experience, neuromodulation and development all changed which process became limiting and which neural system carried the demand.
01 · INHIBITORY CONTEXT
Perceptual similarity between Go and No-go signals impaired inhibition, and physical stimulus intensity changed stopping through response-selection processes in right inferior frontal cortex.[1,2] Semantic conflict could actually improve inhibition by recruiting middle and inferior frontal control systems, illustrating that the same conflict can hinder action execution but facilitate stopping.[3] Overlapping Go and No-go features required unbinding and recoding across parahippocampal and superior-frontal systems.[4]
The sensory modality of conflict changed both behavioural interference and the cortical network used for stopping.[5] Cue validity interacted with inhibitory demand and a person's experience of cue reliability.[6] Even subliminal conflict depended on early attentional and task-set processes rather than only on later conflict monitoring.[7] A consensus guide translated such boundary conditions into rigorous recommendations for stop-signal-task design and analysis.[8]
In plain terms: Inhibition is not an isolated brake; its success depends on how information is perceived, predicted and recoded before the motor command is stopped.
02 · HIDDEN AND VISIBLE INFORMATION
Conscious and subliminal conflicts increased frontal theta power but differed in their effect on large-scale network efficiency: non-conscious conflict selectively reduced theta-network efficiency.[9] Resting theta set the sensitivity of later conflict-modulated inhibition, while 1/f neural noise decreased when control was recruited and covaried with norepinephrine-related processing.[10,11]
The content of a task mattered beyond conflict paradigms. Numerical task switching placed different demands on parietal processing for parity and magnitude judgments.[12] Synaesthesia showed that even objectively absent but subjectively real percepts can guide action through higher-order perception-response translation.[13]
In plain terms: Whether information is conscious, expected or even objectively present changes the route by which it influences action.
03 · NEUROMODULATION AND METACONTROL
Methylphenidate effects on inhibition depended jointly on prior task experience and working-memory load.[14] Anodal stimulation could remove norepinephrine-related modulation of superior-frontal theta, showing that two interventions may interact rather than add up.[15] Genetic differences in catecholamine synthesis separated conscious from subliminal conflict, with norepinephrine contributing particularly to the latter.[16]
Dopamine D1 receptor efficiency was beneficial mainly under high control requirements, consistent with a stable task-set or persistence state.[17] Cholinergic receptor variation changed the use of prior information during flexibility.[18] Dopamine-related genetic variation also predicted self-reported action control differently by sex, adding a trait-level perspective to the state-dependent experiments.[19]
In plain terms: A neurochemical factor is rarely good or bad in isolation; its effect depends on the type and intensity of the control problem.
04 · DEVELOPMENT AND CLINICAL DIVERSITY
Tourette syndrome showed stronger perception-action binding that directly altered inhibition.[20] Deep learning separated children with ADHD from controls using event-related EEG, while mechanistic analyses revealed a hierarchical organization of inhibitory subprocesses that was altered in ADHD.[21,22] Adolescents with OCD could show a paradoxical stopping advantage because strong frontostriatal activation benefited a particular combination of automatic and controlled processes.[23]
In cerebellar ataxia, forward-model generation was relatively preserved but updating and error awareness were disturbed.[24] Thalamic GABA appeared to support compensatory control in restless legs syndrome.[25] Across adolescence, sequential flexibility remained less efficient and relied on different perceptual-categorization and frontal processes than in adults.[26]
In plain terms: Behavioural success can conceal compensation, while behavioural difficulty can arise from very different representational and neurochemical pathways.
05 · ALCOHOL AND STIMULANT USE
A hangover produced only a small impairment in response selection and spared inhibition.[27] After prolonged methamphetamine abstinence, response selection could be behaviourally intact even when other executive domains remained vulnerable.[28] Frequent binge drinking by itself was not associated with measurable deficits in inhibition or flexibility.[29]
Acute high-dose alcohol presented a different picture: task switching deteriorated, especially through impaired cue processing and increased later control demand, although practice attenuated part of the effect.[30] These boundary conditions prevented broad substance-related labels from replacing process-specific explanation.
In plain terms: Substance exposure does not weaken every executive function equally; timing, dose, experience and the particular operation being tested determine the observed deficit.
In 2019, context became part of the mechanism. Perception, awareness, expectation, task experience and neurobiology determined how control was implemented. This process-level view explained both counterintuitive advantages and selective impairments, and it made experimental design itself central to the interpretation of inhibition.
Curated from PubMed records returned for Beste C[au] in 2019. Citation numbers in the story link to entries below. DOI links open the publisher landing page; PubMed links open the indexed record.
Adelhöfer N, Chmielewski WX, Beste C. Journal of neurophysiology. 2019;122(2):500-511.
DOI: 10.1152/jn.00298.2019 · PubMed
Friedrich J, Mückschel M, Beste C. Behavioural brain research. 2019;359:597-608.
DOI: 10.1016/j.bbr.2018.10.006 · PubMed
Chmielewski WX, Beste C. Journal of cognitive neuroscience. 2019;31(9):1430-1442.
DOI: 10.1162/jocn_a_01424 · PubMed
Chmielewski WX, Beste C. NeuroImage. 2019;196:227-236.
DOI: 10.1016/j.neuroimage.2019.04.035 · PubMed
Friedrich J, Beste C. Neuroscience. 2019;410:191-201.
DOI: 10.1016/j.neuroscience.2019.05.010 · PubMed
Adelhöfer N, Beste C. Brain structure & function. 2019;224(5):1911-1924.
DOI: 10.1007/s00429-019-01884-y · PubMed
Bensmann W, Vahid A, Beste C, Stock AK. Frontiers in human neuroscience. 2019;13:53.
DOI: 10.3389/fnhum.2019.00053 · PubMed
Verbruggen F, Aron AR, Band GP, Beste C, et al.. eLife. 2019;8:e46323.
DOI: 10.7554/eLife.46323 · PubMed
Bensmann W, Zink N, Mückschel M, Beste C, Stock AK. Brain structure & function. 2019;224(5):1697-1709.
DOI: 10.1007/s00429-019-01866-0 · PubMed
Pscherer C, Mückschel M, Summerer L, Bluschke A, Beste C. Human brain mapping. 2019;40(14):4253-4265.
DOI: 10.1002/hbm.24699 · PubMed
Pertermann M, Mückschel M, Adelhöfer N, Ziemssen T, Beste C. Journal of neurophysiology. 2019;121(5):1633-1643.
DOI: 10.1152/jn.00701.2018 · PubMed
Petruo VA, Mückschel M, Beste C. Cortex; a journal devoted to the study of the nervous system and behavior. 2019;120:101-115.
DOI: 10.1016/j.cortex.2019.03.017 · PubMed
Schreiter ML, Chmielewski WX, Ward J, Beste C. Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2019;374(1787):20180574.
DOI: 10.1098/rstb.2018.0574 · PubMed
Bensmann W, Zink N, Roessner V, Stock AK, Beste C. Journal of psychopharmacology (Oxford, England). 2019;33(6):678-687.
DOI: 10.1177/0269881119827815 · PubMed
Adelhöfer N, Mückschel M, Teufert B, Ziemssen T, Beste C. Brain structure & function. 2019;224(3):1291-1300.
DOI: 10.1007/s00429-019-01839-3 · PubMed
Bensmann W, Zink N, Arning L, Beste C, Stock AK. Molecular neurobiology. 2019;56(12):8087-8100.
DOI: 10.1007/s12035-019-01664-z · PubMed
Zink N, Bensmann W, Arning L, Colzato LS, Stock AK, Beste C. The international journal of neuropsychopharmacology. 2019;22(12):747-753.
DOI: 10.1093/ijnp/pyz024 · PubMed
Zink N, Bensmann W, Arning L, Stock AK, Beste C. Molecular neurobiology. 2019;56(9):6134-6141.
DOI: 10.1007/s12035-019-1521-6 · PubMed
Schlüter C, Arning L, Fraenz C, Friedrich P, et al.. Social cognitive and affective neuroscience. 2019;14(7):759-768.
DOI: 10.1093/scan/nsz049 · PubMed
Petruo V, Bodmer B, Brandt VC, Baumung L, Roessner V, Münchau A, Beste C. Journal of child psychology and psychiatry, and allied disciplines. 2019;60(9):953-962.
DOI: 10.1111/jcpp.12938 · PubMed
Vahid A, Bluschke A, Roessner V, Stober S, Beste C. Journal of clinical medicine. 2019;8(7):1055.
DOI: 10.3390/jcm8071055 · PubMed
Chmielewski W, Bluschke A, Bodmer B, Wolff N, Roessner V, Beste C. Developmental cognitive neuroscience. 2019;36:100623.
DOI: 10.1016/j.dcn.2019.100623 · PubMed
Wolff N, Chmielewski W, Buse J, Roessner V, Beste C. NeuroImage. Clinical. 2019;23:101893.
DOI: 10.1016/j.nicl.2019.101893 · PubMed
Tunc S, Baginski N, Lubs J, Bally JF, et al.. NeuroImage. Clinical. 2019;24:102043.
DOI: 10.1016/j.nicl.2019.102043 · PubMed
Zhang R, Werner A, Hermann W, Brandt MD, Beste C, Stock AK. Neuroscience letters. 2019;712:134494.
DOI: 10.1016/j.neulet.2019.134494 · PubMed
Giller F, Zhang R, Roessner V, Beste C. Human brain mapping. 2019;40(2):552-565.
DOI: 10.1002/hbm.24394 · PubMed
Opitz A, Hubert J, Beste C, Stock AK. Journal of clinical medicine. 2019;8(9):1317.
DOI: 10.3390/jcm8091317 · PubMed
Bensmann W, Ernst J, Rädle M, Opitz A, Beste C, Stock AK. Frontiers in psychiatry. 2019;10:823.
DOI: 10.3389/fpsyt.2019.00823 · PubMed
Bensmann W, Kayali ÖF, Beste C, Stock AK. Progress in neuro-psychopharmacology & biological psychiatry. 2019;93:93-101.
DOI: 10.1016/j.pnpbp.2019.03.019 · PubMed
Zink N, Zhang R, Chmielewski WX, Beste C, Stock AK. Progress in neuro-psychopharmacology & biological psychiatry. 2019;89:97-108.
DOI: 10.1016/j.pnpbp.2018.08.034 · PubMed