Deficits in Inhibitory Control in Smokers During a Go/NoGo Task: An Investigation Using Event-Related Brain Potentials

Franken IHA (2011) Deficits in Inhibitory Control in Smokers During a Go/NoGo Task: An Investigation Using Event-Related Brain Potentials. PLoS ONE 6(4): e18898. doi:10.1371/journal.pone.0018898 Deficits in Inhibitory Control in Smokers During a Go/NoGo Task: An Investigation Using Event-Related Brain Potentials Maartje Luijten 0 Marianne Littel 0 Ingmar H. A. Franken 0 Antonio Verdejo Garca, University of Granada, Spain 0 Institute of Psychology, Erasmus University Rotterdam , Rotterdam , The Netherlands Introduction: The role of inhibitory control in addictive behaviors is highlighted in several models of addictive behaviors. Although reduced inhibitory control has been observed in addictive behaviors, it is inconclusive whether this is evident in smokers. Furthermore, it has been proposed that drug abuse individuals with poor response inhibition may experience greater difficulties not consuming substances in the presence of drug cues. The major aim of the current study was to provide electrophysiological evidence for reduced inhibitory control in smokers and to investigate whether this is more pronounced during smoking cue exposure. Methods: Participants (19 smokers and 20 non-smoking controls) performed a smoking Go/NoGo task. Behavioral accuracy and amplitudes of the N2 and P3 event-related potential (ERP), both reflecting aspects of response inhibition, were the main variables of interest. Results: Reduced NoGo N2 amplitudes in smokers relative to controls were accompanied by decreased task performance, whereas no differences between groups were found in P3 amplitudes. This was found to represent a general lack of inhibition in smokers, and not dependent on the presence of smoking cues. Conclusions: The current results suggest that smokers have difficulties with response inhibition, which is an important finding that eventually can be implemented in smoking cessation programs. More research is needed to clarify the exact role of cue exposure on response inhibition. - Several contemporary models of addiction highlight the role of impulsivity and executive functioning in the development and maintenance of addiction [18]. A core component of executive functioning is response inhibition which is generally defined as the ability to adaptively suppress behavior when environmental contingences demand this [9]. It has been proposed that poor response inhibition in substance-dependent individuals is associated with difficulties to resist the consumption of a substance especially when exposed to highly salient substance-related cues [1]. Reduced response inhibition has been observed in several substances dependent patient populations including alcohol [10], cocaine [11], and opioid [12] dependent patients. Some studies have also investigated response inhibition in smokers. In these studies, inhibitory control was generally assessed by means of behavioral paradigms, such as Go/NoGo tasks. In the Go/NoGo task, participants have to respond as quickly as possible to frequently occurring Go stimuli, and to inhibit responses to infrequent NoGo stimuli. Results of studies on response inhibition in smokers have been inconsistent. That is, some studies have found response inhibition during a Go/NoGo task to be impaired in smokers relative to controls [13] whereas other studies did not find this group difference in performance on the Go/ NoGo task [14], nor on other behavioral tasks measuring response inhibition [15,16]. The recording of electroencephalographic (EEG) activity during response inhibition has been suggested to yield more sensitive indices (i.e., event-related potentials, ERPs) of response inhibition and may therefore clarify the inconsistent results. Two major ERP components have been reported to be enhanced for NoGo trials as compared to Go trials suggesting that these reflect changes in brain activity related to response inhibition in a Go/NoGo task. The first of these ERP-components is the NoGo N2 which is a negative wave that emerges approximately 200300 ms after stimulus presentation and has maximum peaks on frontal scalp sites. Mounting evidence suggests that the NoGo N2 amplitude is a valuable measure for response inhibition. The NoGo N2 amplitude has been consistently found to be related to behavioral outcomes of inhibitory control on Go/NoGo tasks [17] irrespective of the stimulus modality used in these tasks [18,19]. Although, Go and NoGo trials differ with respect to the overt motor response, which could influence the difference between Go and NoGo N2 amplitudes, it has been found that theNoGo N2 is not restricted to tasks requiring these overt motor responses [20], furthermore a modulation of the N2 ERP by response inhibition requirements has been observed in other inhibition-related paradigms besides the Go/NoGo task [2123]. The second ERP component that has been associated with response inhibition research, is the NoGo P3 which is a positive wave that emerges circa 300500 ms after stimulus onset and has a more central distribution. There are some concerns about the exact role or meaning of P3 amplitudes in response inhibition processes [17,24]. In contrast to the NoGo N2, the NoGo P3 does not seem to be consistently related to response inhibition on a behavioral level. However, some studies show a clear relationship between NoGo P3 amplitude and behavioral outcomes of response inhibition tasks [20,25]. Moreover, because the P3 is a rather late ERP-component (.300 ms) it has been suggested that it does not reflect the initial reflexive stage of the inhibition process but rather a later stage of the inhibition process that is closely related to the actual inhibition of the motor system in the premotor cortex [21,26]. In any event, both decreased NoGo P3 and N2 amplitudes have been reported in various populations with reduced inhibitory control such as children with ADHD [27,28] and impulsive violent offenders [29] suggesting that both ERP components are adequate indices of inhibitory processes in impulsive populations. Few studies have used ERPs to investigate response inhibition with ERPs in substance-dependent patients [3034] and, to our knowledge, only one of these studies has focused on smokers [33]. Remarkably, with the exception of the study by Yang et al. [32], analyses of all these studies were confined to the P3 amplitude whereas studies in other psychiatric populations have usually investigated both the N2 and P3 amplitudes [2729,3540]. ERP studies investigating response inhibition in substance-dependent patients have generally found NoGo P3 amplitudes to be reduced [31,33,34] as compared to healthy controls. However, in heroin patients only the NoGo N2 amplitude appeared to be reduced; no differences were found on the NoGo P3 [32]. All the above-mentioned studies investigated general response inhibition in addicted individuals by using affectively neutral task paradigms. It has been proposed, however, that the reactivity to conditioned (...truncated)