Is impulsivity related to attentional bias in cigarette smokers? An exploration across levels of nicotine dependency and deprivation.

Research has largely focused on how attentional bias to smoking-related cues and impulsivity independently influence the development and maintenance of cigarette smoking, with limited exploration of the relationship between these mechanisms. The current experiments systematically assessed relationships between multiple dimensions of impulsivity and attentional bias, at different stages of attention, in smokers varying in nicotine dependency and deprivation. Nonsmokers (NS; n  = 26), light-satiated smokers (LS; n  = 25), heavy-satiated smokers (HS; n  = 23) and heavy 12-hour nicotine-deprived smokers (HD; n  = 30) completed the Barratt Impulsivity Scale, delayed discounting task, stop-signal task, information sampling task and a visual dot-probe assessing initial orientation (200 ms) and sustained attention (2000 ms) toward smoking-related cues. Sustained attention to smoking-related cues was present in both HS and LS, while initial orientation bias was only evident in HS. HS and LS also had greater levels of trait motor and nonplanning impulsivity and heightened impulsive choice on the delay discounting task compared with NS, while heightened trait attentional impulsivity was only found in HS. In contrast, in HD, nicotine withdrawal was associated with no attentional bias but heightened reflection impulsivity, poorer inhibitory control and significantly lower levels of impulsive choice relative to satiated smokers. Trait and behavioral impulsivity were not related to the extent of attentional bias to smoking-related cues at any stage of attention, level of nicotine dependency or state of deprivation. Findings have both clinical and theoretical implications, highlighting the unique and independent roles impulsivity and attentional bias may play at different stages of the nicotine addiction cycle.

Disentangling the effects of cannabis and cigarette smoking on impulsivity.

BACKGROUND: Cannabis smoking and cigarette smoking often co-occur, yet limited research has investigated the potentially different role impulsivity may play when these behaviours occur in isolation, compared with in combination. AIMS: This study examined trait and behavioural impulsivity as a function of both cigarette and cannabis smoking. METHODS: Trait impulsivity (BIS-11) was compared between 44 non-smokers, 76 cigarette only, 47 cannabis only and 58 cannabis plus cigarette smokers. The effects of cigarette and cannabis smoking on behavioural impulsivity (stop-signal and information sampling tasks) were then assessed in 87 of these participants during a laboratory session. RESULTS: Trait impulsivity was significantly higher in cigarette smokers than non-smokers, irrespective of cannabis use, except for motor impulsivity, where cigarette smoking was only associated with elevated trait impulsivity in non-smokers of cannabis. Dimensions of trait impulsivity were significantly positively related to cigarette smoking frequency and nicotine dependence, but not to cannabis smoking frequency or dependence. Smoking cigarettes or cannabis was associated with significantly impaired reflection impulsivity relative to not smoking either substance. However, no additional increases in reflection impulsivity were observed in those who smoked both cigarettes and cannabis. No group differences in response inhibition were detected. CONCLUSIONS: Heightened trait impulsivity appears to be uniquely related to cigarette smoking, whilst the smoking of cigarettes or cannabis is associated with impairments in reflection impulsivity. Improved outcomes for treating cannabis dependence may result from encouraging concomitant cigarette smokers to cease using both drugs simultaneously in order to reduce heightened impulsivity and risk of relapse.

Dissociating wanting and anticipated liking from consummatory liking in smokers with different levels of nicotine dependence.

INTRODUCTION: Incentive Sensitisation theory suggests wanting and liking are dissociable concepts, with wanting, but not liking typically increasing with repeated drug use. Wanting is associated with anticipation of reward, whereas liking relates to pleasure derived from consummatory behaviour. However, numerous studies have conceptualised liking as an anticipatory cognition. This study explores whether levels of nicotine dependence differentially effect wanting and liking responses to smoking-related cues, and whether anticipated and consummatory liking are equivalent, and dissociable from wanting. METHOD: Heavy (HS, mean = 16 cigarettes/day) and light non-daily (LS, mean = 2 cigarettes/day) smokers completed wanting and anticipated liking questionnaires pre-, immediately post-exposure to smoking-related and neutral cues and at session-end. Consummatory liking was measured post-session, immediately after smoking. RESULTS: Wanting and anticipated liking responses were comparable. Smoking-related cues increased wanting and anticipated liking compared to neutral cues. This effect was maintained until session-end. No baseline differences were seen between HS and LS on wanting or anticipated liking, however after cue exposure, and at session-end, HS reported greater drug wanting and anticipated liking than LS. Conversely, HS and LS did not differ on consummatory liking. Analyses confirmed the relationship between wanting and anticipated liking was significantly stronger than wanting and consummatory liking or anticipated and consummatory liking. CONCLUSIONS: Wanting and anticipated liking appear to be overlapping constructs assessing expectations of reward, that are dissociable from consummatory liking. Furthermore, heavier smoking increases drug wanting, but not smoking pleasure. Future attempts to dissociate these concepts should ensure liking is measured during/immediately after consumption.

Acute nicotine increases both impulsive choice and behavioural disinhibition in rats.

RATIONALE: Heavy smokers exhibit greater levels of impulsive choice and behavioural disinhibition than non-smokers. To date, however, the relationship between nicotine use and differing dimensions of impulsivity has not been systematically assessed. OBJECTIVES: A series of studies was designed to assess the acute dose-response effects of nicotine and the nicotinic receptor antagonist mecamylamine alone, and in combination with nicotine, on impulsive choice and behavioural disinhibition in rats. METHODS: Separate groups of rats were trained on a symmetrically reinforced go/no-go task to measure levels of disinhibition and a systematic delayed reward task to measure levels of impulsive choice. Once trained, all animals in each task were treated acutely with nicotine (0.125, 0.25, 0.5 and 1.0 mg/kg), mecamylamine (0.1, 0.3 and 1.0 mg/kg) and varying doses of mecamylamine (0.1, 0.3 and 1.0 mg/kg) prior to nicotine (0.5 mg/kg). An additional experiment assessed the effects of alterations in primary motivation (presatiation and fasting) on performance in both tasks. RESULTS: Acute nicotine increased both impulsive choice and behavioural disinhibition, effects that were blocked by pre-treatment with mecamylamine. Mecamylamine when administered alone did not alter impulsive behaviour. The lack of effect of presatiation on performance measures suggests that the observed nicotine-induced impulsivity cannot be attributed to the anorectic activity of the compound. CONCLUSIONS: Present findings support the hypothesis that heightened impulsivity in smokers may in part be a consequence of the direct acute effects of nicotine. As such, drug-induced changes in impulsivity may play a critical role in the transition to and maintenance of nicotine dependence.

Paroxetine combined with a 5-HT(1A) receptor antagonist reversed reward deficits observed during amphetamine withdrawal in rats.

RATIONALE: "Diminished interest or pleasure" in rewarding stimuli is an affective symptom of amphetamine withdrawal and a core symptom of depression. An operational measure of this symptom is elevation of brain stimulation reward thresholds during drug withdrawal. Data indicated that increasing serotonin neurotransmission by co-administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine and the serotonin-1A receptor antagonist p-MPPI reversed reward deficits observed during drug withdrawal (Harrison et al. 2001). OBJECTIVES: We tested the hypothesis that increased serotonergic and noradrenergic neurotransmission, using the SSRI paroxetine which also inhibits noradrenaline reuptake, would alleviate affective aspects of amphetamine withdrawal. METHODS: A discrete-trial, current-threshold, self-stimulation procedure was used to assess brain reward function. The effects of paroxetine and p-MPPI alone and in combination were assessed in non-drug-withdrawing animals. We assessed also the effects of paroxetine and p-MPPI alone and in combination on reward deficits associated with amphetamine withdrawal. RESULTS: Paroxetine or p-MPPI alone had no effect on thresholds, while the co-administration of p-MPPI (3 mg/kg) and paroxetine (1.25 mg/kg) elevated thresholds in non-withdrawing rats. Amphetamine withdrawal resulted in threshold elevations. The co-administration of p-MPPI and paroxetine reduced the duration of amphetamine-withdrawal-induced reward deficits. CONCLUSIONS: Increased serotonergic and noradrenergic neurotransmission decreased reward function in non-withdrawing rats, while the same treatment reversed reward deficits associated with amphetamine withdrawal. Considering that paroxetine acts on both the serotonin and noradrenaline transporter, these results indicate that the affective symptoms of amphetamine withdrawal, similar to non-drug-induced depressions, may be, in part, mediated through reduced serotonergic and noradrenergic neurotransmission.

Nicotine potentiation of brain stimulation reward reversed by DH beta E and SCH 23390, but not by eticlopride, LY 314582 or MPEP in rats.

RATIONALE: Systemic nicotine administration increases dopamine and glutamate levels in reward-related brain areas. Nicotine-induced increases of dopamine in the nucleus accumbens are in part mediated by glutamatergic projections to the ventral tegmental area dopamine neurons. OBJECTIVES: To assess the effects of actions at acetylcholine, dopamine, presynaptic (mGluR(2/3)) and postsynaptic (mGluR(5)) metabotropic glutamate receptors (mGluRs) on the potentiation of brain stimulation reward induced by systemically administered nicotine (0.125-0.5 mg/kg; free base) in rats. METHODS: A discrete-trial current-threshold s stimulation reward procedure (electrodes placed in the posterior lateral hypothalamus) was used to assess the effects of DH beta E (0.5-5 mg/kg), an acetylcholine nicotinic receptor antagonist, SCH 23390 (1.25-5 microg/kg), a dopamine D(1) receptor antagonist, eticlopride (2.5-20 microg/kg), a dopamine D(2) receptor antagonist, LY 314582 (1-20 mg/kg), an mGluR(2/3) agonist, and MPEP (1-9 mg/kg), an mGluR(5) antagonist, on the reward potentiating effects of nicotine (0.25 mg/kg). RESULTS: DH beta E had no effect on reward thresholds when administered alone, but dose-dependently reversed the nicotine-induced potentiation of brain stimulation reward. SCH 23390 (5 microg/kg) elevated thresholds when administered alone, and reversed the nicotine-induced potentiation of brain stimulation reward even at a dose (2.5 microg/kg) that had no effect on reward thresholds. Eticlopride (10-20 microg/kg), LY 314582 (10-20 mg/kg) and MPEP (9 mg/kg) elevated thresholds when administered alone but had no effect on the nicotine-induced potentiation of brain stimulation reward. CONCLUSIONS: These results indicate that nicotinic and dopamine D(1) receptors are involved in the nicotine-induced potentiation of brain stimulation reward, while actions at dopamine D(2), mGlu(2/3) and mGlu(5) receptors did not modulate this effect of nicotine.