趙 鑫 劉曉婷 昝香怡 周愛保

(1西北師范大學心理學院,行為康復訓練研究中心,蘭州 730070)(2蘭州大學第二醫(yī)院VIP呼吸科,蘭州 730070)

1 引言

近期的研究發(fā)現(xiàn),吸煙會對個體的認知功能造成一定程度的影響(Billieux et al.,2010;Buzzell,Fedota,Roberts,&McDonald,2014;Gray et al.,2014;Impey,Chique-Alfonzo,Shah,Fisher,&Knott,2013;Luijten et al.,2011a;Spinella,2002)。研究者認為,這是由于煙草中的尼古丁會影響大腦的執(zhí)行功能(executive function,EF)(Ashare,Falcone,&Lerman,2014;Dawkins,Powell,West,Powell,&Pickering,2007;Heishman,Kleykamp,&Singleton,2010;Livingstone et al.,2009)。執(zhí)行功能作為大腦的高級認知功能,對一系列的認知與行為起到了關(guān)鍵的作用。反應抑制是一種重要的執(zhí)行功能(Clark,1996),指抑制已經(jīng)形成的動作反應,是對行動的抑制(抑制優(yōu)勢反應或反應傾向)過程,是執(zhí)行控制的一個關(guān)鍵組成部分(Johnstone,Barry,Markovska,Dimoska,&Clarke,2009)。更具體的說,反應抑制就是抑制不再需要或不恰當?shù)男袨?以便個體可以對外界環(huán)境進行各種靈活的和有目的的行為反應(Verbruggen&Logan,2009)。另外,這一能力對于結(jié)束不再相關(guān)任務、改正錯誤、依據(jù)變化改變原有任務等具有重要意義(Aron&Poldrack,2006)。一些研究表明,與不吸煙者相比,吸煙者的反應抑制功能會受到所攝入的尼古丁的影響(Charles-Walsh,Furlong,Munro,&Hester,2014;Luijten et al.,2011a;Monterosso,Aron,Cordova,Xu,&London,2005)。研究者大多采用Go/NoGo任務(Buzzell et al.,2014;Dinn,Aycicegi,&Harris,2004;Evans,Park,Maxfield,&Drobes,2009;Impey et al.,2013;Longo,Fried,Cameron,&Smith,2013;Luijten et al.,2011a;Rass,Fridberg,&O’Donnell,2014;Spinella,2002)和停止信號任務(Stop-Signal tasks,SST)(Billieux et al.,2010;de Ruiter,Oosterlaan,Veltman,vanden Brink,& Goudriaan,2012;Logemann, B?cker, Deschamps, Kemner, &Kenemans,2014;Monterosso et al.,2005;Rass et al.,2014;Reynolds et al.,2007)對吸煙者的反應抑制能力進行評估。吸煙者反應抑制能力的研究對于探明煙草成癮者以及尼古丁依賴者執(zhí)行功能受影響的深層原因及機制有一定的價值。臨床上,對于煙草成癮者的干預與治療也具有重要的實踐意義。本文在總結(jié)相關(guān)研究的基礎(chǔ)上,闡述吸煙對反應抑制能力影響的證據(jù)、原因以及所存在的爭議,以期對該領(lǐng)域的研究提供新的視角。

2 吸煙對反應抑制能力的影響——來自行為、ERPs、腦成像的研究

目前,許多研究者采用行為實驗(Billieux et al.,2010;Powell,Pickering,Dawkins,West,&Powell,2004;Reynolds et al.,2007)、事件相關(guān)電位(event-related potentials,ERPs)技術(shù)(Buzzell et al.,2014;Impey et al.,2013;Luijten et al.,2011a,b)以及功能磁共振成像(functional magenetic resonance imaging,fMRI)技術(shù)(de Ruiter et al.,2012;Ettinger et al.,2009;Gray et al.,2014;Hartwell et al.,2011;Longo et al.,2013;Luijten et al.,2013)研究發(fā)現(xiàn),吸煙會對個體的反應抑制能力產(chǎn)生影響。

2.1 行為研究

在行為層面上,研究者采用Go/NoGo任務和Stop-Signal任務發(fā)現(xiàn),吸煙者的虛報率(Commission error)和反應時兩個指標都顯著高于正常健康對照組被試(Billieux et al.,2010;de Ruiter et al.,2012;Nestor,McCabe,Jones,Clancy,&Garavan,2011;Reynolds et al.,2007)。虛報率是對不需要做出反應的非目標刺激做出的反應,是衡量反應抑制能力的一個重要的行為指標(Thorell,Lindqvist,Bergman Nutley,Bohlin,&Klingberg,2009),研究者認為吸煙者在Go/NoGo任務和Stop-Signal任務中虛報率較高的原因在于吸煙者的大腦執(zhí)行功能受到所攝入的尼古丁的影響(Bekker,B?cker,van Hunsel,van Den Berg,&Kenemans,2005;Billieux et al.,2010;Luijten et al.,2011a)。目前,大量的研究者對吸煙者與不吸煙者的反應抑制能力進行比較研究時采用線索反應模式(Brody,Mandelkern,&Jarvik,et al.,2004;Luijten et al.,2011a,b;Mogg,Bradley,Field,&De Houwer,2003;Munafò,Mogg,Roberts,Bradley,& Murphy,2003;Sayette&Hufford,1994;Waters&Feyerabend,2000),線索反應模式通過向個體呈現(xiàn)物理刺激來誘發(fā)其渴求,其中又分為真實刺激(Sayette&Hufford,1994)、視頻刺激(Baumann&Sayette,2006;Brody et al.,2002;Monterosso et al.,2005;Tong,Bovbjerg,&Erblich,2007)、圖片刺激(Hitsman et al.,2008;Luijten et al.,2011b)、聽覺刺激和腳本/想象刺激(Epstein,Temple,Roemmich,&Bouton,2009;Soetens,Braet,Dejonckheere,& Roets,2006;Wegner,1992)。有關(guān)吸煙者反應抑制的研究通過呈現(xiàn)經(jīng)過評定后的標準化圖片,采用最明顯的視覺刺激的方式來誘發(fā)吸煙者的渴求。Luijten等人(2011a)采用Go/NoGo任務對吸煙者與正常健康被試的對照研究表明,吸煙者在NoGo刺激上的虛報率顯著高于正常對照組。另外,有研究采用Stop-Signal任務對輕度吸煙者和中度吸煙者的對照研究表明,中度吸煙者(吸煙量平均每天11～20支)對Stop信號的抑制反應時間更長,成功抑制比例更低(Bekker et al.,2005;Billieux et al.,2010)。另外,Rass等人(2014)通過對連續(xù)吸煙者、間斷吸煙者和不吸煙者的反應抑制能力進行比較發(fā)現(xiàn),連續(xù)吸煙者的反應抑制潛伏期顯著小于間斷吸煙者和正常健康被試。有研究者采用Stop-Signal任務對戒煙時間不同的吸煙者和正常被試的反應抑制對比研究發(fā)現(xiàn),吸煙者在戒煙時間較長(10小時)情況下其反應抑制能力受到一定程度的影響,正常健康對照組被試的停止任務績效顯著高于吸煙群體,即正常群體的抑制成功率高,停止信號反應時(SSRT)短(Charles-Walsh et al.,2014;Logemann et al.,2014;Monterosso et al.,2005)。

2.2 ERPs研究

研究者從行為層面上發(fā)現(xiàn),與不吸煙者相比,吸煙者的反應抑制能力受到所攝入的尼古丁的影響(Bekker et al.,2005;Billieux et al.,2010;Charles-Walsh etal.,2014;Dawkins,Powell,Pickering,Powell,&West,2009;Logemann et al.,2014;Rass et al.,2014)。研究者們還采用事件相關(guān)電位技術(shù)揭示了吸煙對反應抑制加工過程的影響(Buzzell et al.,2014;Impey et al.,2013;Logemann et al.,2014;Luijten et al.,2011a)。Luijten等人(2011a)比較了19名吸煙者和20名不吸煙的健康被試在Go/NoGo任務中的ERPs成分,結(jié)果顯示,吸煙者的NoGo-N2波幅顯著低于正常健康被試,而吸煙組和不吸煙組在NoGo-P3成分上未表現(xiàn)出顯著差異。Buzzell等人(2014)的研究支持了上述結(jié)果,該研究以大學本科生為被試,檢測了15名輕度吸煙者和15名不吸煙者的ERPs成分,研究發(fā)現(xiàn),輕度吸煙組的NoGo-N2波幅明顯小于正常對照組,而兩組被試的NoGo-P3成分無顯著差異。一般認為,NoGo-N2主要定位于前扣帶回(Bekker,Kenemans,&Verbaten,2005;Dimoska,Johnstone,&Barry,2006;Nieuwenhuis,Yeung,van Den Wildenberg,&Ridderinkhof,2003;Yeung,Botvinick,&Cohen,2004)和右側(cè)眶額葉(Strik,Fallgatter,Brandeis,& Pascual-Marqui,1998);NoGo-P3定位于眶額葉(Bokura,Yamaguchi,&Kobayashi,2001)。盡管兩者的心理過程沒有最終確定,但是可以認為,NoGo-N2和NoGo-P3可能分別代表了與抑制控制有關(guān)的兩個加工過程,反應抑制和沖突監(jiān)控(Ruchsow et al.,2008)。有觀點認為NoGo-N2反映了一種自上而下的抑制機制(Falkenstein,Hoormann,&Hohnsbein,1999),即在運動執(zhí)行前抑制不適當?shù)姆磻獌A向(Kok,Ramautar,De Ruiter,Band,&Ridderinkhof,2004),這種早期加工的異常很可能反應了吸煙者在運動執(zhí)行前抑制不適當?shù)姆磻獌A向上受到所攝入的尼古丁的影響(Luijten et al.,2011a)。

2.3 腦成像研究

近期,對吸煙者反應抑制能力的腦成像研究發(fā)現(xiàn),與不吸煙者相比,吸煙者丘腦(Thalamic)、額中回(Middle frontal gyrus)和前扣帶回(Anterior cingulate cortex)灰質(zhì)體積減小(Brody,Mandelkern,&Lee et al.,2004;Gallinat et al.,2006)。另外, 腦成像研究還發(fā)現(xiàn),吸煙者額葉(諸如ACC、PFC和OFC)、枕葉和顳葉,包括海馬旁回腦區(qū)的灰質(zhì)體積明顯減小、密度明顯降低。丘腦、小腦和黑質(zhì)的灰質(zhì)體積或密度也發(fā)生了變化(Gallinat et al.,2006)。吸煙者的丘腦灰質(zhì)體積減少可能與尼古丁對吸煙者認知功能的影響有關(guān)(Sharma&Brody,2009)。有研究發(fā)現(xiàn),吸煙者在對與吸煙有關(guān)的刺激進行反應抑制時,與不吸煙者相比,吸煙者眶額葉皮層(Orbitofrontal cortex OFC)、前額皮層(Prefrontal cortex PFC)和前扣帶回皮層(ACC)的激活增強(Hartwell et al.,2011;McBride,Barrett,Kelly,Aw,& Dagher,2006;Wilson,Sayette,Delgado,&Fiez,2005)。Brody 等(2002)采用正電子發(fā)射斷層掃描(Positron Emission Tomography PET)技術(shù)對重度吸煙者和非吸煙者呈現(xiàn)與香煙相關(guān)線索的錄像作為香煙渴求誘發(fā)刺激,間隔10天對被試進行香煙相關(guān)線索和中性線索作用下的兩次掃描,結(jié)果發(fā)現(xiàn)嚴重吸煙者比非吸煙者在扣帶回前部、顳葉和眶額皮層的葡萄糖代謝增加更多。

綜上所述,研究者借用行為、ERPs和腦成像研究手段,發(fā)現(xiàn)了吸煙可能會對反應抑制能力產(chǎn)生影響的證據(jù)。但是,一些ERPs和腦成像研究的結(jié)果只能說明吸煙者與不吸煙者在反應抑制導致的腦激活上存在差異,這僅能作為吸煙影響反應抑制能力的間接證據(jù),還不能完全揭示二者之間的因果關(guān)系。之后的研究應關(guān)注腦激活數(shù)據(jù)與行為數(shù)據(jù)的聯(lián)合分析,以進一步探討吸煙與反應抑制能力損傷之間的因果關(guān)系。

3 吸煙對反應抑制能力影響的原因

3.1 吸煙對前額葉系統(tǒng)的影響

吸煙者表現(xiàn)出較差的反應抑制能力,可能是因為吸煙者在尼古丁的長期作用下,認知控制網(wǎng)絡等相關(guān)腦區(qū)受到影響,導致吸煙個體不能使用情景預期來指導選擇,最終導致反應抑制能力下降(Cole et al.,2010)。由于額葉是執(zhí)行和控制行為的主要腦區(qū)(Fowler,Volkow,Kassed,&Chang,2007),而成癮者最大的特征是不能控制自己反復使用成癮物質(zhì)的行為(Volkow,Fowler,&Wang,2003)。因此,吸煙對抑制控制能力的影響可能與額葉某個或某些腦區(qū)活動改變有關(guān)。而腦成像研究表明,尼古丁依賴者的前額腦區(qū)異常(Brody,Mandelkern,&Jarvik,et al.,2004;Carroll,Sutherland,Salmeron,Ross,&Stein,2014;Gallinat et al.,2006;Luijten et al.,2013)。前額葉(Prefrontal cortex,PFC)系統(tǒng)主要由眶額葉皮層(Orbital frontal cortex,OFC)、前扣帶回皮層(Anterior cingulate cortex,ACC)、背外側(cè)前額葉皮層(Dorsolateral prefrontal cortex,DLPFC)、腹外側(cè)前額葉皮層(Ventrolateral prefrontal cortex,VLPFC)、額下回(Inferior frontal gyrus,IFG)等部分組成,對個體的抑制控制功能發(fā)揮著重要作用(Egner,2011)。與不吸煙者相比,吸煙者反應抑制能力的減弱與前額葉系統(tǒng)的失調(diào)息息相關(guān)(Ettinger et al.,2009;Fregni et al.,2008;Gallinat et al.,2006;Spinella,2002)。有研究者發(fā)現(xiàn),與正常健康被試相比,吸煙者前額葉與前扣帶回皮層、前額葉與眶額葉皮層的功能連接下降(Luijten et al.,2013);背外側(cè)前額皮質(zhì)(DLPFC)和腹外側(cè)前額葉皮質(zhì)(VLPFC)的皮層灰質(zhì)體積和密度明顯減小,而且吸煙者左半球背側(cè)前扣帶回(Dorsal anterior cingulate cortex D-ACC)的灰質(zhì)體積和右半球小腦的灰質(zhì)密度降低(Brody,Mandelkern,&Jarvik,et al.,2004);前額葉(PFC)和前扣帶回皮層(ACC)的神經(jīng)反應性活動也減弱了(Riggs et al.,2007)。背外側(cè)前額葉皮質(zhì)與前扣帶回皮層、眶額葉皮層及其前額葉腦區(qū)的功能連接受損,導致吸煙者大腦功能出現(xiàn)異常,從而表現(xiàn)出反應抑制能力下降。

3.2 吸煙對中腦邊緣多巴胺系統(tǒng)的影響

中腦邊緣多巴胺系統(tǒng)(mesolimbic dopamine system MLDS)是腦內(nèi)獎賞或強化系統(tǒng)的主要結(jié)構(gòu),其獎賞回路由腹側(cè)被蓋區(qū)(Ventral Tegmental Area,VTA)、伏隔核(Nucleus Accumbens,NAc)和杏仁核(Amygdala)等構(gòu)成(王惠玲,趙晏,2003),它是包括尼古丁在內(nèi)的很多成癮物質(zhì)的中介系統(tǒng)(鄧林園,方曉義,2005)。有研究發(fā)現(xiàn),在藥物依賴者服藥期間,從中腦腹側(cè)被蓋區(qū)神經(jīng)元末稍釋放的多巴胺增加,而且,這些藥物通過不同的靶位激活中腦邊緣多巴胺系統(tǒng),這種激活增加了中腦腹側(cè)被蓋區(qū)的多巴胺神經(jīng)元的放電,隨后增加多巴胺遞質(zhì)釋放到伏隔核和前額葉皮層等邊緣前腦的其他腦區(qū)(張開鎬,2002)。

fMRI研究表明,當給被試靜脈注射尼古丁后發(fā)現(xiàn),尼古丁引起伏隔核、杏仁核、扣帶回以及額葉等腦區(qū)神經(jīng)活動的增強(Stein et al.,1998)。另外,有研究采用fMRI技術(shù)探測發(fā)現(xiàn),被試暴露于香煙相關(guān)線索時,尼古丁依賴者中腦邊緣多巴胺系統(tǒng)和前額葉皮層均得到激活,并且報告渴求感增強(Due,Huettel,Hall,&Rubin,2002;Hitsman et al.,2008)。

在動物成癮方面,研究者用老鼠進行的活體內(nèi)微透析實驗結(jié)果發(fā)現(xiàn)尼古丁使用可以導致中腦腹側(cè)被蓋區(qū)(VTA)的多巴胺釋放明顯增多(Rahman,Zhang,&Corrigall,2003)。Yin和 French等(2000)的研究也發(fā)現(xiàn)尼古丁顯著增加了多巴胺神經(jīng)元的神經(jīng)脈沖放電。上述研究表明中腦邊緣多巴胺系統(tǒng)和尼古丁依賴息息相關(guān),在尼古丁直接刺激或者尼古丁渴求誘發(fā)線索刺激作用下,所激活的腦區(qū)基本上都是中腦邊緣多巴胺系統(tǒng)以及相關(guān)的腦區(qū)。Mansvelder,Keath和McGehee(2002)研究發(fā)現(xiàn)尼古丁引起腹側(cè)被蓋區(qū)內(nèi)γ－氨基丁酸(γ-aminobutyric acid,GABA)傳遞的抑制。

γ-氨基丁酸主要作用是抑制多巴胺細胞并且對其它結(jié)構(gòu)產(chǎn)生影響,比如腳橋被蓋核、谷氨酸能的神經(jīng)元等。尼古丁通過直接誘導多巴胺的釋放或抑制GABA能神經(jīng)元,最終導致腹側(cè)被蓋區(qū)的多巴胺輸入端向伏隔核釋放多巴胺的持續(xù)增強(Picciotto&Corrigall,2002)。正常情況下,多巴胺神經(jīng)元還受到通過腹側(cè)被蓋區(qū)的GABA中間神經(jīng)元以及包括伏隔核和蒼白球在內(nèi)的其他腦區(qū)投射來的GABA纖維的抑制性控制。但是,它們在接觸尼古丁后很快就會出現(xiàn)去敏化,結(jié)果將導致向DA神經(jīng)元的抑制性輸入減弱,這樣一來,對多巴胺神經(jīng)元的抑制就解除了,使釋放到伏隔核區(qū)的多巴胺量增加。有研究發(fā)現(xiàn),吸煙者的快感體驗與多巴胺水平的增加有關(guān)(Brody et al.,2006)。這表明尼古丁的攝入使個體產(chǎn)生陶醉感和愉悅感,就算是短時間地偶爾吸煙也足以使人產(chǎn)生尼古丁或香煙依賴。

4 吸煙對反應抑制能力影響的爭議

如前所述,雖然有大量的研究發(fā)現(xiàn)吸煙對反應抑制能力有影響(Glass et al.,2009;Billieux et al.,2010;de Ruiter et al.,2012;Luijten et al.,2011a,b;Spinella,2002),但是,另外一些研究卻并未發(fā)現(xiàn)這一現(xiàn)象(Dinn et al.,2004;Galván,Poldrack,Baker,McGlennen,&London,2011;Rass et al.,2014;Luijten et al.,2013;Monterosso et al.,2005;Rass et al.,2014;Reynolds et al.,2007)。例如,Buzzell等人(2014)選取吸煙者與不吸煙者作為被試,比較兩組被試在Go/NoGo任務中Go試次的漏報率和NoGo試次的虛報率,研究結(jié)果發(fā)現(xiàn),吸煙者與不吸煙者在行為結(jié)果上未表現(xiàn)出差異;Evans等人(2009)的研究也發(fā)現(xiàn),吸煙者在NoGo試次的正確率以及Go試次的反應時兩個指標上與不吸煙者相比沒有差異?？梢?目前對吸煙是否影響個體的反應抑制能力還存在爭議。研究結(jié)果產(chǎn)生爭議的原因可能主要有以下三點：

第一,研究者采用的實驗范式不同所得出的結(jié)論可能會有差異。在已有研究中,研究者通常使用Stop-Signal任務和Go/NoGo任務對吸煙者反應抑制進行研究。例如,Buzzell等(2014)使用Go/NoGo任務對吸煙者和非吸煙者的反應抑制能力進行研究發(fā)現(xiàn),兩組被試在行為反應上無明顯差異。Logemann等人(2014)利用Stop-Signal任務對吸煙者的行為抑制能力進行了評估,他們發(fā)現(xiàn)吸煙者對Go刺激的反應速度與正常對照組相比沒有明顯差別,但吸煙者的SSRT卻明顯延長。Stop-Signal和Go/NoGo兩種任務所依賴的加工機制不完全相同,在Stop-Signal任務中,要停止的反應已經(jīng)處于加工過程之中,加工已經(jīng)到達相當水平,遠遠高出了對NoGo刺激的加工。對此有研究發(fā)現(xiàn),基底神經(jīng)節(jié)(basal ganglia)在Stop-Signal任務中對動作反應的發(fā)起和抑制有重要作用(Eagle&Robbins,2003),基底神經(jīng)節(jié)是前腦中的一組皮質(zhì)下神經(jīng)核,包括尾狀核、殼核、蒼白球、丘腦底核(subthalamic nucleus STN)和中腦黑質(zhì)(Alexander&Crutcher,1990)。在基底神經(jīng)節(jié)的神經(jīng)核中,丘腦底核可能是參與反應抑制加工的關(guān)鍵結(jié)構(gòu)(Cohen&Frank,2009;Ray et al.,2012;Wiecki&Frank,2013)。Aron和 Poldrack(2006)研究了丘腦底核和SSRT之間的關(guān)系,研究發(fā)現(xiàn)丘腦底核激活越強,被試的SSRT越短。即：SSRT較短的被試丘腦底核激活強于SSRT較長的被試。對吸煙者與不吸煙者的腦機制結(jié)構(gòu)進行對比發(fā)現(xiàn),與不吸煙者相比,吸煙者的丘腦、小腦和黑質(zhì)的灰質(zhì)體積或密度減小,既然反應和不反應之間的競爭主要在基底神經(jīng)節(jié)的神經(jīng)核中進行,刺激或損傷這些神經(jīng)核將會對反應抑制產(chǎn)生明顯影響(Chambers et al,2006;2007)。此外,有研究發(fā)現(xiàn)Go/NoGo任務所激活左側(cè)大腦的其它一些區(qū)域,如前扣帶回、前運動輔助區(qū)等都與高水平的運動計劃及行為選擇相關(guān),而在Stop-Signal任務中,前額葉皮層、基底神經(jīng)節(jié)、額下回等都參與了反應停止操作(Rubia et al.,2001)。這表明,較之Stop-Signal任務,Go/NoGo任務中的抑制更多涉及行為的選擇和行為的準備。

第二,實驗任務的難度不同也可能影響實驗結(jié)果。研究發(fā)現(xiàn),Go/NoGo任務的難度取決于Go刺激和NoGo刺激的呈現(xiàn)時間以及NoGo刺激所占的比率(Evans et al.,2009;Luijten et al.,2011a)。例如,Evans等人(2009)采用的Go/NoGo任務中刺激呈現(xiàn)時間為800 ms,整個實驗共包括900個trial,其中83個NoGo trial,在此研究中發(fā)現(xiàn)吸煙者在NoGo試次的正確率以及Go試次的反應時兩個指標上與不吸煙者相比沒有差異。而Luijten等人(2011a)采用的Go/NoGo任務中刺激呈現(xiàn)時間為200ms,整個實驗共包括 400個trial,其中NoGo試次占所有試次的25%,該研究得出了相反的結(jié)論,即吸煙者在NoGo試次的正確率上顯著低于不吸煙者。因此我們認為,采取相同的Go/NoGo任務,刺激呈現(xiàn)的時間和NoGo試次所占的比例不同影響了上述實驗結(jié)果的不一致。對這一實驗結(jié)果有研究發(fā)現(xiàn),背外側(cè)前額葉與前扣帶回在反應抑制中的激活隨工作記憶負荷增加而增強,Simmonds,Pekar和 Mostofsky(2008)對 10項使用Go/NoGo范式研究反應抑制能力的fMRI研究的元分析發(fā)現(xiàn),與簡單的抑制任務相比,工作記憶負荷較高的復雜抑制任務更多的激活了額中回(middle frontal gyrus),額下回(inferior frontal gyrus),頂下小葉(inferior parietal lobule)和顳-頂交界處(temporoparietal junction TPJ),頂下小葉和前額皮質(zhì)有密切的雙向纖維聯(lián)系,對執(zhí)行控制至關(guān)重要。但是,這些腦區(qū)只在復雜任務條件下同時激活。與這種解釋一致,有研究發(fā)現(xiàn)在增加工作記憶負荷的Go/NoGo任務中背外側(cè)前額皮層激活增強,而簡單Go/NoGo任務中該區(qū)并無激活增強(Rowe,Friston,Frackowiak,&Passingham,2002)。但是,與不吸煙者相比,吸煙者背外側(cè)前額皮質(zhì)(DLPFC)和腹外側(cè)前額葉皮質(zhì)(VLPFC)的皮層灰質(zhì)體積和密度明顯減小(Brody,Mandelkern,&Jarvik,et al.,2004),因此,吸煙者與不吸煙者相比,在難度較大的Go/NoGo任務中吸煙者在NoGo刺激上的正確率顯著小于正常對照組。

第三,所選取的吸煙被試的吸煙成癮程度也可能是影響實驗結(jié)果的一個重要因素。例如,有研究者選取輕度吸煙和不吸煙的大學生作為被試,采用Go/NoGo任務對正常健康被試和輕度吸煙被試的反應抑制能力進行比較研究發(fā)現(xiàn),輕度吸煙組被試和正常健康組被試在Go的反應時和NoGo的正確率兩個指標上均未表現(xiàn)出差異(Buzzell et al.,2014;Evans et al.,2009);但是,Luijten等人(2011a)選取19名中度吸煙和20名不吸煙的大學本科生作為被試,采用Go/NoGo任務對兩組被試的反應抑制能力進行比較,研究結(jié)果發(fā)現(xiàn),中度吸煙者在NoGo試次的正確率上顯著低于不吸煙者,而且與不吸煙者相比,中度吸煙者的NoGo-N2波幅顯著低于正常健康被試。這說明,吸煙組的成癮程度可能會影響到實驗結(jié)果。當前,有些研究已證明吸煙的成癮程度與個體的反應抑制能力有關(guān)。如,Spinella(2002)采用Go/NoGo任務研究發(fā)現(xiàn),被試在實驗中犯錯誤的概率與每天吸煙的數(shù)量呈正相關(guān);Billieux等人(2010)的研究也發(fā)現(xiàn)吸煙者反應抑制的個體差異與每天抽煙的數(shù)量有關(guān)。研究認為,對優(yōu)勢反應的抑制能力越差,吸煙成癮程度越重,相反,對優(yōu)勢反應的抑制能力越好其吸煙成癮程度越輕。Robinson,Pritchard和Davis(1992)比較了吸低尼古丁含量(0.06 mg)和高尼古丁含量(0.6 mg)的香煙前后EEG的變化,發(fā)現(xiàn)在控制了吸煙量和吸煙強度的條件下,尼古丁含量為 0.6mg的香煙引起EEG的激活,但0.06mg的沒有。

5 展望

雖然許多研究者從行為到神經(jīng)機制對吸煙成癮人群的反應抑制能力展開了大量研究,但還存在眾多疑問,今后可以著重從以下幾個方面進行研究。

第一,盡管不同研究者都對尼古丁激活大腦前額葉系統(tǒng)和中腦邊緣多巴胺系統(tǒng)這一事實達成一致,但刺激方式局限于視覺或視聽覺,且對具體激活腦區(qū)及核團的定位尚存在較大爭議,這可能是因為在進行掃描時選擇的被試吸煙成癮程度以及所處的渴求狀態(tài)不同所致。因此,將來的研究可以對處于不同的香煙剝奪狀態(tài)(如剛吸完一支煙與吸煙后2小時這兩種不同狀態(tài))下的吸煙者的反應抑制能力進行對比研究,同時,還可以比較不同類型的人群,包括香煙成癮者、香煙成癮戒斷者以及不吸煙者之間在香煙或者香煙相關(guān)線索刺激下反應抑制能力及其大腦活動的變化情況,從而使香煙成癮機制的研究更精確也更全面。

第二,尼古丁依賴同其他依賴性藥物機制之間的差異至今沒有太多研究者有所涉及;因而,用同樣的研究模式和手段,對毒品、酒精和香煙等常見依賴性藥物在藥物直接刺激或相關(guān)的環(huán)境線索作用下大腦活動狀況的異同進行分析,找出吸煙者反應抑制能力受損的特異性,從而為香煙成癮的戒斷發(fā)展出更有針對性的干預方案。

第三,到目前為止,對反應抑制能力的研究主要采用Go/NoGo任務和Stop-Signal任務。但是,由于Go/NoGo任務要求只對Go刺激反應,對NoGo刺激并不反應,這樣可能導致在Go/NoGo范式中觀察到的抑制控制效應已被反應相關(guān)加工污染,并且難以提取反應時間,常常不能為反應抑制提供有效的行為指標(Yuan,He,Qinglin,Chen,&Li,2008);Stop-Signal任務雖然能提供行為指標,但行為抑制信號在時間上的不確定性容易混淆抑制信號和任務信號誘發(fā)的腦活動。近年來有研究者將雙選擇oddball范式用來進行反應抑制能力的研究(Yuan et al.,2008;Yuan et al.,2012)。雙選擇oddball范式是對傳統(tǒng)oddball范式的改編,該范式要求被試既快又準的對大概率的標準刺激和小概率的偏差刺激做兩類不同的按鍵反應。由于標準刺激的呈現(xiàn)概率遠大于偏差刺激,因此,被試對標準刺激的反應將成為優(yōu)勢反應,當偏差刺激出現(xiàn)時,被試需要抑制對標準刺激的優(yōu)勢反應,從而確保對偏差刺激做出正確的行為反應。而偏差刺激反應時與標準刺激反應時之差則為反應抑制的行為學指標(辛勇,李紅,袁加錦,2010)。因此,在以后的研究中可以使用雙選擇oddball范式對吸煙者的反應抑制能力與不吸煙者進行對比研究,并且比較Go/NoGo范式、Stop-Signal范式以及雙選擇oddball范式在行為、ERPs和腦成像上所得結(jié)果的異同,為以后進行反應抑制能力的研究提供更有效的研究范式。

最后,開發(fā)改善吸煙人群反應抑制缺陷的干預方法與技術(shù)。對吸煙成癮人群反應抑制缺陷的認知與神經(jīng)機制的研究,最終是為了改善和治療吸煙成癮人群的反應抑制缺陷。然而,對于這方面的干預方法與技術(shù)的研究才剛剛起步。研究表明,預期想象訓練和金錢管理指導能夠在一定程度上降低吸煙成癮人群的反應抑制缺陷(Martin-Soelch et al.,2001;Powell et al.,2004)。但是,目前這些方法與技術(shù)都還處于研究階段,離真正的臨床治療階段還較遠。因此,需要不斷細化、完整這些方法和技術(shù),使其有更好的操作性、規(guī)范性和臨床效果。

鄧林園,方曉義.(2005).尼古丁依賴的神經(jīng)生物學機制.心理科學進展,13(4),534–543.

王惠玲,趙晏.(2003).阿片類藥物依賴與中腦-邊緣多巴胺系統(tǒng)回路.中國藥物依賴性雜志,12(1),2–5.

辛勇,李紅,袁加錦.(2010).負性情緒干擾行為抑制控制:一項事件相關(guān)電位研究.心理學報,42(3),334–341.

張開鎬.(2002).藥物成癮的病理生理學基礎(chǔ).中國藥物依賴性雜志,11(2),81–82.

Alexander,G.E.,&Crutcher,M.D.(1990).Functional architecture of basal ganglia circuits:Neural substrates of parallel processing.Trends in Neurosciences,13(7),266–271.

Aron,A.R.,&Poldrack,R.A.(2006).Cortical and subcortical contributions to stop signal response inhibition:Role of the subthalamic nucleus.The Journal of Neuroscience,26(9),2424–2433.

Ashare,R.L.,Falcone,M.,&Lerman,C.(2014).Cognitive function during nicotine withdrawal:Implicationsfor nicotine dependence treatment.Neuropharmacology,76,581–591.

Baumann,S.B.,&Sayette,M.A.(2006).Smoking cues in a virtualworld provoke craving in cigarette smokers.Psychology of Addictive Behaviors,20(4),484–489.

Bekker,E.M.,B?cker,K.B.E.,van Hunsel,F.,van den Berg,M.C.,&Kenemans,J.L.(2005).Acute effects of nicotine on attention and response inhibition.Pharmacology Biochemistry and Behavior,82(3),539–548.

Bekker,E.M.,Kenemans,J.L.,&Verbaten,M.N.(2005).Source analysis of the N2 in a cued Go/NoGo task.Cognitive Brain Research,22(2),221–231.

Billieux,J.,Gay,P.,Rochat,L.,Khazaal,Y.,Zullino,D.,&van der Linden,M.(2010).Lack of inhibitory control predicts cigarette smoking dependence:Evidence from a non-deprived sample of light to moderate smokers.Drug and Alcohol Dependence,112(1-2),164–167.

Bokura,H.,Yamaguchi,S.,& Kobayashi,S.(2001).Electrophysiological correlates for response inhibition in a Go/NoGo task.Clinical Neurophysiology,112(12),2224–2232.

Brody,A.L.,Mandelkern,M.A.,Jarvik,M.E.,Lee,G.S.,Smith,E.C.,Huang,J.C.,…London,E.D.(2004).Differences between smokers and nonsmokers in regional gray matter volumes and densities.Biological Psychiatry,55(1),77–84.

Brody,A.L.,Mandelkern,M.A.,Lee,G.,Smith,E.,Sadeghi,M.,Saxena,S.,… London,E.D.(2004).Attenuation of cue-induced cigarette craving and anterior cingulate cortex activation in bupropion-treated smokers:A preliminary study.Psychiatry Research:Neuroimaging,130(3),269–281.

Brody,A.L.,Mandelkern,M.A.,London,E.D.,Childress,A.R.,Lee,G.S.,Bota,R.G.,&Madsen,D.(2002).Brain metabolic changes during cigarette craving.Archives of General Psychiatry,59(12),1162–1172.

Brody,A.L.,Mandelkern,M.A.,Olmstead,R.E.,Scheibal,D.,Hahn,E.,Shiraga,S.,&London,E.D.(2006).Gene variants ofbrain dopamine pathways and smokinginduced dopamine release in the ventral caudate/nucleus accumbens.Archives of General Psychiatry,63(7),808–816.

Buzzell,G.A.,Fedota,J.R.,Roberts,D.M.,&McDonald,C.G.(2014).The N2 ERP component as an index of impaired cognitive controlin smokers.Neuroscience Letters,563,61–65.

Carroll,A.J.,Sutherland,M.T.,Salmeron,B.J.,Ross,T.J.,&Stein,E.A.(2014).Greater externalizing personality traits predict less error-related insula and anterior cingulate cortex activity in acutely abstinent cigarette smokers.Addiction Biology,20(2),377–389.

Chambers,C.D.,Bellgrove,M.A.,Gould,I.C.,English,T.,Garavan,H.,McNaught,E.M.,…Mattingley,J..(2007).Dissociable mechanisms of cognitive control in prefrontal and premotor cortex.Journal of Neurophysiology,98(6),3638–3647.

Chambers,C.D.,Bellgrove,M.A.,Stokes,M.G.,Henderson,T.R.,Garavan,H.,Robertson,I.H.,…Mattingley,J.B.(2006).Executive ‘brake failure’following deactivation of human frontal lobe.Journal of Cognitive Neuroscience,18(3),444–455.

Charles-Walsh,K.,Furlong,L.,Munro,D.G.,&Hester,R.(2014).Inhibitory control dysfunction in nicotine dependence and the influence of short-term abstinence.Drug and Alcohol Dependence,143(1),81–86.

Clark,J.M.(1996).Contributions of inhibitory mechanisms to unified theory in neuroscience and psychology.Brain and Cognition,30(1),127–152.

Cohen,M.X.,&Frank,M.J.(2009).Neurocomputational models of basal ganglia function in learning,memory and choice.Behavioural Brain Research,199(1),141–156.

Cole,D.M.,Beckmann,C.F.,Long,C.J.,Matthews,P.M.,Durcan,M.J.,&Beaver,J.D.(2010).Nicotine replacement in abstinentsmokers improves cognitive withdrawal symptomswith modulation ofresting brain network dynamics.NeuroImage,52(2),590–599.

Dawkins,L.,Powell,J.H.,Pickering,A.,Powell,J.,&West,R.(2009).Patterns of change in withdrawal symptoms,desire to smoke,reward motivation and response inhibition across 3 months of smoking abstinence.Addiction,104(5),850–858.

Dawkins,L.,Powell,J.H.,West,R.,Powell,J.,&Pickering,A.(2007).A double-blind placebo-controlled experimental study of nicotine:II—Effects on response inhibition and executive functioning.Psychopharmacology,190(4),457–467.

de Ruiter,M.B.,Oosterlaan,J.,Veltman,D.J.,van den Brink,W.,&Goudriaan,A.E.(2012).Similar hyporesponsiveness of the dorsomedial prefrontal cortex in problem gamblers and heavy smokers during an inhibitory control task.Drug and Alcohol Dependence,121(1–2),81–89.

Dimoska,A.,Johnstone,S.J.,&Barry,R.J.(2006).The auditory-evoked N2 and P3 components in the stop-signal task:Indices of inhibition,response-conflict or error-detection?Brain and Cognition,62(2),98–112.

Dinn,W.M.,Aycicegi,A.,&Harris,C.L.(2004).Cigarette smoking in a student sample:Neurocognitive and clinical correlates.Addictive Behaviors,29(1),107–126.

Due,D.L.,Huettel,S.A.,Hall,W.G.,&Rubin,D.C.(2002).Activation in mesolimbic and visuospatial neural circuits elicited by smoking cues:Evidence from functional magnetic resonance imaging.American Journal of Psychiatry,159(6),954–960.

Eagle,D.M.,&Robbins,T.W.(2003).Lesions of the medial prefrontal cortex or nucleus accumbens core do not impair inhibitory control in rats performing a stop-signal reaction time task.Behavioural Brain Research,146(1–2),131–144.

Egner,T.(2011).Rightventrolateralprefrontalcortex mediates individual differences in conflict-driven cognitive control.Journal of Cognitive Neuroscience,23(12),3903–3913.

Epstein,L.H.,Temple,J.L.,Roemmich,J.N.,&Bouton,M.E.(2009).Habituation as a determinant of human food intake.Psychological Review,116(2),384–407.

Ettinger,U.,Williams,S.C.,Patel,D.,Michel,T.M.,Nwaigwe,A.,Caceres,A.,&Kumari,V.(2009).Effects of acute nicotine on brain function in healthy smokers and non-smokers:Estimation of inter-individual response heterogeneity.NeuroImage,45(2),549–561.

Evans,D.E.,Park,J.Y.,Maxfield,N.,&Drobes,D.J.(2009).Neurocognitive variation in smoking behavior and withdrawal:Genetic and affective moderators.Genes,Brain and Behavior,8(1),86–96.

Falkenstein,M.,Hoormann,J.,&Hohnsbein,J.(1999).ERP componentsin Go/Nogo tasks and theirrelation to inhibition.Acta Psychologica,101(2-3),267–291.

Fowler,J.S.,Volkow,N.D.,Kassed,C.A.,&Chang,L.D.(2007).Imaging the addicted human brain.Science&Practice Perspectives,3(2),4–16.

Fregni,F.,Liguori,P.,Fecteau,S.,Nitsche,M.A.,Pascual-Leone,A.,& Boggio,P.S.(2008).Cortical stimulation of the prefrontal cortex with transcranial direct current stimulation reduces cue-provoked smoking craving:A randomized,sham-controlled study.Journal of Clinical Psychiatry,69(1),32–40.

Gallinat,J.,Meisenzahl,E.,Jacobsen,L.K.,Kalus,P.,Bierbrauer,J.,Kienast,T.,& Schubert,F.(2006).Smoking and structural brain deficits:A volumetric MR investigation.European Journal of Neuroscience,24(6),1744–1750.

Galván,A.,Poldrack,R.A.,Baker,C.M.,McGlennen,K.M.,&London,E.D.(2011).Neural correlates of response inhibition and cigarette smoking in late adolescence.Neuropsychopharmacology,36(5),970–978.

Glass,J.M.,Buu,A.,Adams,K.M.,Nigg,J.T.,Puttler,L.I.,Jester,J.M.,& Zucker,R.A.(2009).Effects of alcoholism severity and smoking on executive neurocognitive function.Addiction,104(1),38–48.

Gray,J.C.,Amlung,M.T.,Acker,J.,Sweet,L.H.,Brown,C.L.,&MacKillop,J.(2014).Clarifying the neural basis for incentive salience of tobacco cues in smokers.Psychiatry Research:Neuroimaging,223(3),218–225.

Hartwell,K.J.,Johnson,K.A.,Li,X.,Myrick,H.,LeMatty,T.,George,M.S.,& Brady,K.T.(2011).Neural correlates of craving and resisting craving for tobacco in nicotine dependent smokers.Addiction Biology,16(4),654–666.

Heishman,S.J.,Kleykamp,B.A.,&Singleton,E.G.(2010).Meta-analysis of the acute effects of nicotine and smoking on human performance.Psychopharmacology,210(4),453–469.

Hitsman,B.,MacKillop,J.,Lingford-Hughes,A.,Williams,T.M.,Ahmad,F.,Adams,S.,&Munafò,M.R.(2008).Effects of acute tyrosine/phenylalanine depletion on the selective processing ofsmoking-related cuesand the relative value of cigarettes in smokers.Psychopharmacology,196(4),611–621.

Impey,D.,Chique-Alfonzo,M.,Shah,D.,Fisher,D.J.,&Knott,V.J.(2013).Effects of nicotine on visuospatial attentional orienting in non-smokers.Pharmacology Biochemistry and Behavior,106,1–7.

Johnstone,S.J.,Barry,R.J.,Markovska,V.,Dimoska,A.,&Clarke,A.R.(2009).Response inhibition and interference control in children with AD/HD:A visual ERP investigation.International Journal of Psychophysiology,72(2),145–153.

Kok,A.,Ramautar,J.R.,De Ruiter,M.B.,Band,G.P.,&Ridderinkhof,K.R.(2004).ERP components associated with successful and unsuccessful stopping in a stop-signal task.Psychophysiology,41(1),9–20.

Livingstone,P.D.,Srinivasan,J.,Kew,J.N.,Dawson,L.A.,Gotti,C.,Moretti,M.,&Wonnacott,S.(2009).α7 and non-α7 nicotinic acetylcholine receptors modulate dopamine release in vitro and in vivo in the rat prefrontal cortex.European Journal of Neuroscience, 29(3),539–550.

Logemann,H.,B?cker,K.,Deschamps,P.,Kemner,C.,&Kenemans,J.L.(2014).The effect of the augmentation of cholinergic neurotransmission by nicotine on EEG indices of visuospatial attention.Behavioural Brain Research,260,67–73.

Longo,C.A.,Fried,P.A.,Cameron,I.,&Smith,A.M.(2013).The long-term effects of prenatal nicotine exposure on response inhibition:An fMRI study of young adults.Neurotoxicology and Teratology,39,9–18.

Luijten,M.,Littel,M.,&Franken,I.H.A.(2011a).Deficits in inhibitory control in smokers during a Go/NoGo task:An investigation using event-related brain potentials.PloS One,6(4),e18898.

Luijten,M.,van Meel,C.S.,&Franken,I.H.(2011b).Diminished error processing in smokers during smoking cue exposure.Pharmacology Biochemistry and Behavior,97(3),514–520.

Luijten,M.,Veltman,D.J.,Hester,R.,Smits,M.,Nijs,I.M.,Pepplinkhuizen,L.,&Franken,I.H.(2013).The role of dopamine in inhibitory control in smokers and non-smokers:A pharmacological fMRI study.European Neuropsychopharmacology,23(10),1247–1256.

Mansvelder,H.D.,Keath,J.R.,&McGehee,D.S.(2002).Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas.Neuron,33(6),905–919.

Martin-Soelch,C.,Leenders,K.L.,Chevalley,A.F.,Missimer,J.,Künig,G.,Magyar,S.,… Schultz,W.(2001).Reward mechanisms in the brain and their role in dependence:Evidence from neurophysiologicaland neuroimaging studies.Brain Research Reviews,36(2–3),139–149.

McBride,D.,Barrett,S.P.,Kelly,J.T.,Aw,A.,&Dagher,A.(2006).Effects of expectancy and abstinence on the neural response to smoking cues in cigarette smokers:An fMRI study.Neuropsychopharmacology,31(12),2728–2738.

Mogg,K.,Bradley,B.P.,Field,M.,&de Houwer,J.(2003).Eye movements to smoking-related pictures in smokers:Relationship between attentional biases and implicit and explicit measures of stimulus valence.Addiction,98(6),825–836.

Monterosso,J.R.,Aron,A.R.,Cordova,X.,Xu,J.,&London,E.D.(2005).Deficits in response inhibition associated with chronic methamphetamine abuse.Drug and Alcohol Dependence,79(2),273–277.

Munafò,M.,Mogg,K.,Roberts,S.,Bradley,B.P.,&Murphy,M.(2003).Selective processing of smoking-related cues in current smokers,ex-smokers and never-smokers on the modified stroop task.Journal of Psychopharmacology,17(3),310–316.

Nestor,L.,McCabe,E.,Jones,J.,Clancy,L.,&Garavan,H.(2011).Differences in “bottom-up”and “top-down”neural activity in current and former cigarette smokers:Evidence for neural substrates which may promote nicotine abstinence through increased cognitive control.NeuroImage,56(4),2258–2275.

Nieuwenhuis,S.,Yeung,N.,van den Wildenberg,W.,&Ridderinkhof,K.R.(2003).Electrophysiological correlates of anterior cingulate function in a go/no-go task:Effects of response conflict and trial type frequency.Cognitive,Affective,&Behavioral Neuroscience,3(1),17–26.

Picciotto,M.R.,&Corrigall,W.A.(2002).Neuronal systems underlying behaviors related to nicotine addiction:Neural circuits and molecular genetics.The Journal of Neuroscience,22(9),3338–3341.

Powell,J.H.,Pickering,A.D.,Dawkins,L.,West,R.,&Powell,J.F.(2004).Cognitive and psychological correlates ofsmoking abstinence,and predictors ofsuccessful cessation.Addictive Behaviors,29(7),1407–1426.

Rahman,S.,Zhang,J.,&Corrigall,W.A.(2003).Effects of acute and chronic nicotine on somatodendritic dopamine release of the ratventraltegmentalarea:In vivo microdialysis study.Neuroscience Letters,348(2),61–64.

Rass,O.,Fridberg,D.J.,&O’Donnell,B.F.(2014).Neural correlates of performance monitoring in daily and intermittent smokers.Clinical Neurophysiology,125(7),1417–1426.

Ray,N.J.,Brittain,J.,Holland,P.,Joundi,R.A.,Stein,J.F.,Aziz,T.Z.,&Jenkinson,N.(2012).The role of the subthalamic nucleus in response inhibition:Evidence from local field potential recordings in the human subthalamic nucleus.NeuroImage,60(1),271–278.

Reynolds,B.,Patak,M.,Shroff,P.,Penfold,R.B.,Melanko,S.,&Duhig,A.M.(2007).Laboratory and self-report assessments of impulsive behavior in adolescent daily smokersand nonsmokers.Experimentaland Clinical Psychopharmacology,15(3),264–271.

Riggs,P.D.,Thompson,L.L.,Tapert,S.F.,Fascella,J.,Mikulich-Culbertson,S.K.,Dalwani,M.,…Lohman,M.(2007).Advances in neurobiological research related to interventions in adolescents with substance use disorders:Research to practice.Drug and Alcohol Dependence,91,306–311.

Robinson,J.H.,Pritchard,W.S.,&Davis,R.A.(1992).Psychopharmacological effects of smoking a cigarette with typical “tar” and carbon monoxide yields but minimal nicotine.Psychopharmacology,108(4),466–472.

Rowe,J.,Friston,K.,Frackowiak,R.,&Passingham,R.(2002).Attention to action:Specific modulation of Corticocortical interactions in humans.NeuroImage,17(2),988–998.

Rubia,K.,Russell,T.,Overmeyer,S.,Brammer,M.J.,Bullmore,E.T.,Sharma,T.,&Andrew,C.M.(2001).Mapping motor inhibition:Conjunctive brain activations across different versions of go/no-go and stop tasks.NeuroImage,13(2),250–261.

Ruchsow,M.,Groen,G.,Kiefer,M.,Buchheim,A.,Walter,H.,Martius,P.,&Ebert,D.(2008).Response inhibition in borderline personality disorder:Event-related potentials in a Go/Nogo task.Journal of Neural Transmission,115(1),127–133.

Sayette,M.A.,&Hufford,M.R.(1994).Effects of cue exposure and deprivation on cognitive resources in smokers.Journal of Abnormal Psychology,103(4),812–818.

Sharma,A.,&Brody,A.L.(2009).In vivo brain imaging of human exposure to nicotine and tobaccoNicotine Psychopharmacology,192,145–171.

Simmonds,D.J.,Pekar,J.J.,&Mostofsky,S.H.(2008).Meta-analysis of Go/No-go tasks demonstrating that fMRI activation associated with response inhibition is task-dependent.Neuropsychologia,46(1),224–232.

Soetens,B.,Braet,C.,Dejonckheere,P.J.N.,&Roets,A.(2006).‘When Suppression Backfires’the ironic effects of suppressing eating-related thoughts.Journal of Health Psychology,11(5),655–668.

Spinella,M.(2002).Correlationsbetween orbitofrontal dysfunction and tobacco smoking.Addiction Biology,7(4),381–384.

Stein,E.A.,Pankiewicz,J.,Harsch,H.H.,Cho,J.,Fuller,S.A.,Hoffmann,R.G.,&Bloom,A.S.(1998).Nicotineinduced limbic cortical activation in the human brain:A functional MRI study.American Journal of Psychiatry,155(8),1009–1015.

Strik,W.K.,Fallgatter,A.J.,Brandeis,D.,&Pascual-Marqui,R.D.(1998).Three-dimensional tomography of event-related potentials during response inhibition:Evidence for phasic frontal lobe activation.Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section,108(4),406–413.

Thorell,L.B.,Lindqvist,S.,Bergman Nutley,S.,Bohlin,G.,&Klingberg,T.(2009).Training and transfer effects of executive functions in preschool children.Developmental Science,12(1),106–113.

Tong, C., Bovbjerg, D. H., & Erblich, J. (2007).Smoking-related videos for use in cue-induced craving paradigms.Addictive Behaviors,32(12),3034–3044.

Verbruggen,F.,&Logan,G.D.(2009).Models of response inhibition in the stop-signal and stop-change paradigms.Neuroscience&Biobehavioral Reviews,33(5),647–661.

Volkow,N.D.,Fowler,J.S.,&Wang,G.J.(2003).The addicted human brain:Insights from imaging studies.The Journal of Clinical Investigation,111(10),1444–1451.

Waters,A.J.,&Feyerabend,C.(2000).Determinants and effects of attentional bias in smokers.Psychology of Addictive Behaviors,14(2),111–120.

Wegner,D.M.(1992).You can’t always think what you want:Problems in the suppression of unwanted thoughts.Advances in Experimental Social Psychology,25,193–225.

Wiecki,T.V.,&Frank,M.J.(2013).A computational model of inhibitory control in frontal cortex and basal ganglia.Psychological Review,120(2),329–355.

Wilson,S.J.,Sayette,M.A.,Delgado,M.R.,&Fiez,J.A.(2005). Instructed smoking expectancy modulates cue-elicited neural activity:A preliminary study.Nicotine&Tobacco Research,7(4),637–645.

Yeung,N.,Botvinick,M.M.,&Cohen,J.D.(2004).The neural basis of error detection:Conflict monitoring and the error-related negativity.Psychological Review,111(4),931–959.

Yin,R.,&French,E.D.(2000).A comparison of the effects of nicotine on dopamine and non-dopamine neurons in the rat ventral tegmental area:Anin vitroelectrophysiological study.Brain Research Bulletin,51(6),507–514.

Yuan,J.J.,He,Y.Y.,Zhang,Q.L.,Chen,A.T.,&Li,H.(2008). Gender differences in behavioral inhibitory control:ERP evidence from a two-choice oddball task.Psychophysiology,45(6),986–993.

Yuan,J.J.,Meng,X.X.,Yang,J.M.,Yao,G.H.,Hu,L.,&Yuan,H.(2012).The valence strength of unpleasant emotion modulates brain processing of behavioral inhibitory control:Neural correlates.Biological Psychology,89(1),240–251.