The neuropsychopharmacology of action inhibition: cross-species translation of the stop-signal and go/no-go tasks

被引:371
作者
Eagle, Dawn M. [1 ]
Bari, Andrea [1 ]
Robbins, Trevor W. [1 ]
机构
[1] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
impulsivity; human; rat; dopamine; noradrenaline; serotonin;
D O I
10.1007/s00213-008-1127-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background and rationale The term 'action inhibition' encapsulates the ability to prevent any form of planned physical response. Growing evidence suggests that different 'stages' or even subtypes of action inhibition activate subtly different neuropharmacological and neuroanatomical processes. Objectives In this review, we present evidence from two commonly used and apparently similar behavioural tests, the stop-signal task and the go/no-go task, to determine if these have similar neuroanatomical and neurochemical modulation. Results Whilst performance of the stop-signal and go/no-go tasks is modulated across only subtly different anatomical networks, serotonin (5-HT) is strongly implicated in inhibitory control on the go/no-go but not the stop-signal task, whereas the stop-signal reaction time appears more sensitive to the action of noradrenaline. Conclusions There is clear neuropharmacological and neuroanatomical evidence that stop-signal and go/no-go tasks represent different forms of action inhibition. This evidence translates with remarkable consistency across species. We discuss the possible implications of this evidence with respect to the development of novel therapeutic treatments for disorders in which inhibitory deficits are prominent and debilitating.
引用
收藏
页码:439 / 456
页数:18
相关论文
共 162 条
[1]   5-HT2C receptor activation by m-chlorophenylpiperazine detected in humans with fMRI [J].
Anderson, IM ;
Clark, L ;
Elliott, R ;
Kulkarni, B ;
Williams, SR ;
Deakin, JFW .
NEUROREPORT, 2002, 13 (12) :1547-1551
[2]   Neurobiology of executive functions: Catecholamine influences on prefrontal cortical functions [J].
Arnsten, AFT ;
Li, BM .
BIOLOGICAL PSYCHIATRY, 2005, 57 (11) :1377-1384
[3]   Stimulants: Therapeutic actions in ADHD [J].
Arnsten, Amy F. T. .
NEUROPSYCHOPHARMACOLOGY, 2006, 31 (11) :2376-2383
[4]   Methylphenidate improves prefrontal cortical cognitive function through α2 adrenoceptor and dopamine D1 receptor actions: Relevance to therapeutic effects in Attention Deficit Hyperactivity Disorder [J].
Arnsten, Amy F. T. ;
Dudley, Anne G. .
BEHAVIORAL AND BRAIN FUNCTIONS, 2005, 1 (1)
[5]   The neural basis of inhibition in cognitive control [J].
Aron, Adam R. .
NEUROSCIENTIST, 2007, 13 (03) :214-228
[6]   Cortical and subcortical contributions to stop signal response inhibition: Role of the subthalamic nucleus [J].
Aron, AR ;
Poldrack, RA .
JOURNAL OF NEUROSCIENCE, 2006, 26 (09) :2424-2433
[7]   The cognitive neuroscience of response inhibition: Relevance for genetic research in attention-deficit/hyperactivity disorder [J].
Aron, AR ;
Poldrack, RA .
BIOLOGICAL PSYCHIATRY, 2005, 57 (11) :1285-1292
[8]   Stop-signal inhibition disrupted by damage to right inferior frontal gyrus in humans [J].
Aron, AR ;
Fletcher, PC ;
Bullmore, ET ;
Sahakian, BJ ;
Robbins, TW .
NATURE NEUROSCIENCE, 2003, 6 (02) :115-116
[9]   Inhibition and the right inferior frontal cortex [J].
Aron, AR ;
Robbins, TW ;
Poldrack, RA .
TRENDS IN COGNITIVE SCIENCES, 2004, 8 (04) :170-177
[10]   Methylphenidate improves response inhibition in adults with attention-deficit/hyperactivity disorder [J].
Aron, AR ;
Dowson, JH ;
Sahakian, BJ ;
Robbins, TW .
BIOLOGICAL PSYCHIATRY, 2003, 54 (12) :1465-1468