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Psychopharmacology (v.194, #2)

Effects of SR141716 and WIN 55,212-2 on tolerance to ethanol in rats using the acute and rapid procedures by Jose Inácio Lemos; Reinaldo Naoto Takahashi; Gina Struffaldi Morato (pp. 139-149).
Our previous findings have shown rapid cross-tolerance between ethanol and Δ9-tetrahydrocannabinol and that intraperitoneal (i.p.) injection of cannabinoid receptor type 1 (CB1R) antagonist SR141716 (SR) does not interfere with tolerance to either of these drugs in mice.This study investigates the effects of SR, alone or in combination with the CB receptor agonist WIN 55,212-2 (WIN), on the development of acute and rapid tolerance to the incoordinating effect of ethanol in rats.Male Wistar rats received SR, through i.p. (0.5–2.0 mg/kg) or intracerebroventricular (i.c.v.) injections (0.5–4.0 μg), alone or together with WIN (1.0 μg, i.c.v.), in combination with ethanol (2.7 g/kg, i.p.). Another group received WIN (1.0 μg, i.c.v.) in combination with ethanol (2.3 g/kg), and the rats were tested for motor coordination. Rapid tolerance was assessed 24 h later by administering ethanol to all animals and retesting them under the same dose regimen. Acute tolerance was evaluated for 75 min after ethanol (3.0 g/kg, i.p.) in animals treated with SR or WIN (i.c.v.).The reduced motor impairment on day 2 (i.e., rapid tolerance) was blocked by SR (i.p. and i.c.v.). WIN (1.0 μg, i.c.v.) facilitated rapid tolerance and also prevented the blockade of rapid tolerance by SR (1.0 μg, i.c.v.). In the acute tolerance procedure, SR did not affect the motor incoordination induced by ethanol.The results suggest that the endocannabinoid system may contribute to the development of rapid tolerance to ethanol.

Keywords: Ethanol; Acute tolerance; Rapid tolerance; Endocannabinoid; SR141716; WIN 55,212-2

Impaired fear recognition in regular recreational cocaine users by L. Kemmis; J. K. Hall; R. Kingston; M. J. Morgan (pp. 151-159).
The ability to read facial expressions is essential for normal human social interaction. The aim of the present study was to conduct the first investigation of facial expression recognition performance in recreational cocaine users.Three groups, comprised of 21 cocaine naïve participants (CN), 30 occasional cocaine (OC), and 48 regular recreational cocaine (RC) users, were compared. An emotional facial expression (EFE) task consisting of a male and female face expressing six basic emotions (happiness, surprise, sadness, anger, fear, and disgust) was administered. Mean percent accuracy and latencies for correct responses across eight presentations of each basic emotion were derived. Participants were also assessed with the “Eyes task” to investigate their ability to recognize more complex emotional states and the Symptom CheckList-90—Revised to measure psychopathology.There were no group differences in psychopathology or “eyes task” performance, but the RC group, who otherwise had similar illicit substance use histories to the OC group, exhibited impaired fear recognition accuracy compared to the OC and CN groups. The RC group also correctly identified anger, fear, happiness, and surprise, more slowly than CN, but not OC participants. The OC group was slower than CN when correctly identifying disgust. The selective deficit in fear recognition accuracy manifested by the RC group cannot be explained by the subacute effects of cocaine, or ecstasy, because recent and less recent users of these drugs within this group were similarly impaired. Possible parallels between RC users and psychopaths with respect to impaired fear recognition, amygdala dysfunction, and etiology are discussed.

Keywords: Cocaine; Fear; Emotion; Facial expression; Amygdala; Psychopath

Cortico-limbic circuitry for conditioned nicotine-seeking behavior in rats involves endocannabinoid signaling by E. Kodas; C. Cohen; C. Louis; G. Griebel (pp. 161-171).
The endocannabinoid system plays an important role in conditioned drug seeking, but the neuronal mechanisms involved in this behavior are unclear.Here, we evaluate the role of endogenous cannabinoids in the cortico-limbic circuitry in cue-induced nicotine-seeking behavior in rats.Animals were first trained to self-administer nicotine (0.03 mg/kg/injection, IV) under conditions in which responding was reinforced jointly by response-contingent nicotine injections and audiovisual stimuli. During subsequent sessions, nicotine was withdrawn and responding was reinforced by contingent presentation of the stimuli only. One month after nicotine removal, the cannabinoid CB1 receptor antagonist, rimonabant, was injected bilaterally into the shell of the nucleus accumbens (ShNAcc, 0.3, 3, or 30 ng/0.5 μl), the basolateral amygdala (BLA, 30 ng/0.5 μl), or the prelimbic cortex (PLCx, 30 ng/0.5 μl).Rimonabant injected into the ShNAcc dose-dependently reduced nicotine-seeking behavior without modifying spontaneous locomotor activity. Similar results were obtained when the drug (30 ng) was injected into the BLA or the PLCx. The anatomical specificity was confirmed in a control experiment using [3H]rimonabant. Fifteen minutes after drug injection, when the behavioral effects of rimonabant were already achieved, radioactivity was detected at the site of injection and had not diffused to adjacent regions.These findings demonstrate that increased endocannabinoid transmission critically triggers conditioned nicotine-seeking behavior in key cortico-limbic regions.

Keywords: Cannabinoid; Nicotine self-administration; Cues; Nucleus accumbens; Basolateral amygdala; Prelimbic cortex

Functional MRI of inhibitory processing in abstinent adolescent marijuana users by Susan F. Tapert; Alecia D. Schweinsburg; Sean P. A. Drummond; Martin P. Paulus; Sandra A. Brown; Tony T. Yang; Lawrence R. Frank (pp. 173-183).
Marijuana intoxication appears to impair response inhibition, but it is unclear if impaired inhibition and associated brain abnormalities persist after prolonged abstinence among adolescent users. We hypothesized that brain activation during a go/no-go task would show persistent abnormalities in adolescent marijuana users after 28 days of abstinence.Adolescents with (n = 16) and without (n = 17) histories of marijuana use were compared on blood oxygen level dependent (BOLD) response to a go/no-go task during functional magnetic resonance imaging (fMRI) after 28 days of monitored abstinence. Participants had no neurological problems or Axis I diagnoses other than cannabis abuse/dependence.Marijuana users did not differ from non-users on task performance but showed more BOLD response than non-users during inhibition trials in right dorsolateral prefrontal, bilateral medial frontal, bilateral inferior and superior parietal lobules, and right occipital gyri, as well as during “go” trials in right prefrontal, insular, and parietal cortices (p < 0.05, clusters > 943 μl). Differences remained significant even after controlling for lifetime and recent alcohol use.Adolescent marijuana users relative to non-users showed increased brain processing effort during an inhibition task in the presence of similar task performance, even after 28 days of abstinence. Thus, increased brain processing effort to achieve inhibition may predate the onset of regular use or result from it. Future investigations will need to determine whether increased brain processing effort is associated with risk to use.

Keywords: Marijuana; Cannabis; Functional magnetic resonance imaging; Adolescence; Response inhibition; Abstinence

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits by Judith A. Siuciak; Sheryl A. McCarthy; A. N. Martin; D. S. Chapin; J. Stock; D. M. Nadeau; S. Kantesaria; D. Bryce-Pritt; S. McLean (pp. 185-195).
The structurally related neuropeptides, substance P, neurokinin A, and neurokinin B, belong to a family of molecules termed tachykinins and are widely distributed in the central and peripheral nervous systems. These peptides mediate their effects through three G protein coupled receptor subtypes, the neurokinin-1, neurokinin-2 and neurokinin-3 receptors, respectively.To study the physiological functions of NK3, a line of NK3 knockout mice were generated and characterized in a broad spectrum of well-established behavioral tests.In several tests, including spontaneous locomotor activity, elevated plus maze, forced swim, and hot plate, wild-type and knockout mice performed similarly. However, in several cognition tests, including passive avoidance, acquisition of conditioned avoidance responding (CAR), and the Morris water maze, NK3 knockout mice displayed deficits compared to wild-type mice. Although NK3 wild-type and knockout mice performed similarly in the training phase of the passive avoidance test, knockout mice had shorter latencies to enter the dark compartment on days 3 and 4, suggesting impaired retention. In the acquisition phase of the conditioned avoidance responding assay, NK3 knockout mice acquired the CAR task at a slower rate than wild-type mice. Once the CAR test was acquired, both NK3 wild-type and knockout mice responded similarly to clozapine and risperidone, drugs which suppress responding in this test. In the Morris water maze, NK3 knockout mice showed increased latencies to find the escape platform on day 3 of training, suggesting a modest, but significant delay in acquisition compared to wild-type mice.These studies suggest a role for NK3 in learning and memory in mice.

Keywords: Knockout; Neurokinin; Tachykinin; Passive avoidance; Morris water maze; Conditioned avoidance; Cognition; Learning; Memory; Schizophrenia

Efficacy and safety of atomoxetine for attention-deficit/hyperactivity disorder in children and adolescents—meta-analysis and meta-regression analysis by Jackie Y. W. Cheng; Ronald Y. L. Chen; John S. N. Ko; Emil M. L. Ng (pp. 197-209).
The objective of this study was to evaluate the efficacy and safety of atomoxetine in children and adolescents.We searched for studies published between 1985 and 2006 through Medline, PubMed, PsychInfo and Cochrane Central Register of Controlled Trials (CENTRAL 2006 Issue 3) using keywords related to atomoxetine and attention-deficit/hyperactivity disorder (ADHD) and scanned though reference lists. We included nine randomized placebo-controlled trials (atomoxetine:placebo = 1,150:678).Atomoxetine was superior (p < 0.01) to placebo in reducing ADHD symptoms across different scales (Attention-Deficit/Hyperactivity Disorder Rating Scale-IV, Conners’ Parent and Teacher Rating Scales-Revised:Short Form, Clinical Global Impression-Severity) rated by different raters (parent, teacher, clinician). The number-needed-to-treat (NNTs) for treatment response and relapse prevention were 3.43 (95% CI, 2.79–4.45) and 10.30 (95% CI, 5.89–40.62), respectively. High baseline ADHD symptoms (p = 0.02) was associated with greater reduction in ADHD symptoms, whereas male gender (p = 0.02), comorbid oppositional defiant disorder (ODD) status (p = 0.01) and ADHD hyperactive/impulsive subtype (p = 0.01) were associated with smaller reductions. The commonest adverse events were gastrointestinal [appetite decrease, number-needed-to-harm (NNH) = 8.81; abdominal pain, NNH = 22.48; vomiting, NNH = 29.96; dyspepsia, NNH = 49.38] and sleep related (somnolence, NNH = 19.41). Young age (p = 0.03) and high baseline hyperactive/impulsive symptoms (p < 0.01) were associated with more adverse events, whereas ADHD inattentive subtype (p = 0.04) was associated with less adverse events. Quality of life using Child Health Questionnaire (CHQ) improved (p < 0.01) with atomoxetine treatment. Both ADHD and ODD symptoms (p < 0.01) were reduced in comorbid ADHD+ODD, and ODD status was not associated with more adverse events. Efficacy and side effects were not altered by comorbid general anxiety disorder or major depression.Atomoxetine is efficacious in reducing ADHD symptoms. It may have a role in treating comorbid ODD or depression, and probably in comorbid anxiety.

Keywords: Atomoxetine; Efficacy; Side effects; Meta-analysis; Meta-regression

Individual differences in elevated plus-maze exploration predicted progressive-ratio cocaine self-administration break points in Wistar rats by David E. A. Bush; Franco J. Vaccarino (pp. 211-219).
There are considerable individual differences in vulnerability to drug addiction, but the mechanisms underlying such differences are poorly understood. Cocaine has potent reinforcing effects that support operant responding. However, cocaine also elicits aversive reactions and produces an approach-avoidance conflict in rats. We hypothesized that preexisting individual differences in open arm exploration on the elevated plus-maze, a well-known model for the study of clinically effective anxiolytic drugs, would predict individual differences in cocaine-motivated behavior.To assess whether individual differences in sensitivity to anxiety-like behavior on the plus-maze predict motivation to self-administer intravenous (i.v.) cocaine.Rats were assessed drug-free for individual differences in open arm exploration on the elevated plus-maze, and later trained to perform an operant response for i.v. cocaine (0, 0.1, 0.3, 0.6, 0.9, 1.2, and 1.5 mg kg−1 infusion−1) on a progressive-ratio reinforcement schedule. Rats were split at the median into low and high open arm explorers based on time spent in the open arms of the plus-maze. Self-administration levels were compared across groups.Rats identified as high open arm explorers on the elevated plus-maze attained higher levels of operant responding for cocaine. Open arm times and break points were significantly correlated at the highest cocaine doses (1.2 and 1.5 mg kg−1 infusion−1).These results indicate that individual differences in anxiety-like behavior on the elevated plus-maze predict motivation to self-administer cocaine, and suggest the possibility that reduced sensitivity to aversive stimuli may be associated with increased vulnerability to the rewarding properties of cocaine.

Keywords: Addiction; Anxiety; Reinforcement; Cocaine; Self-administration; Rat; Operant; Reinforcement

The distinct effects of subchronic antipsychotic drug treatment on macronutrient selection, body weight, adiposity, and metabolism in female rats by M. J. Fell; N. Anjum; K. Dickinson; K. M. Marshall; L. M. Peltola; S. Vickers; S. Cheetham; J. C. Neill (pp. 221-231).
Treatment with some antipsychotic drugs may result in excessive body weight gain which can have detrimental effects on patient compliance, morbidity and mortality. The aim of the present study was to investigate the effect of atypical antipsychotic drugs on dietary macronutrient selection, body weight, body composition and biochemical parameters related to obesity in female rats.Forty pair-housed, adult female hooded-Lister rats (250 ± 5 g) were habituated to three diets containing principally protein, fat, or carbohydrate in a home cage self-selection paradigm. Olanzapine (2 mg/kg), risperidone (0.5 mg/kg), ziprasidone (2.5 mg/kg), or vehicle was injected intraperitoneally once daily for 22 days; food selection, water intake, and body weight were recorded daily, while body composition and plasma hormones (insulin, glucose, nonesterified free fatty acid, total cholesterol, glycerol, triacylglycerol, leptin, and prolactin) were analyzed at the end of the study.Only olanzapine significantly increased body weight and food intake. Macronutrient selection was significantly altered after olanzapine and risperidone treatment (increased protein and decreased fat preference). Only olanzapine increased carcass fat content. Locomotor activity was significantly reduced in all treatment groups. Both olanzapine and risperidone significantly increased plasma prolactin. Olanzapine was without effect on any other biochemical parameter measured. Ziprasidone significantly reduced plasma leptin and nonsignificantly reduced NEFA, while risperidone significantly reduced fasting plasma glucose.This study supports our previous work demonstrating weight gain and increased feeding behavior induced by olanzapine and could have important implications for enhancing our understanding of the mechanisms by which olanzapine and other atypical antipsychotics induce weight gain in the clinic.

Keywords: Antipsychotic; Olanzapine; Risperidone; Ziprasidone; Schizophrenia; Obesity; Rat; Macronutrient selection; Prolactin

A randomized controlled trial of venlafaxine ER and paroxetine in the treatment of outpatients with panic disorder by Mark Pollack; Richard Mangano; Richard Entsuah; Evan Tzanis; Naomi M. Simon (pp. 233-242).
Few randomized, placebo-controlled trials have evaluated the comparative efficacy and tolerability of more than one pharmacological agent for panic disorder.The primary objective of this study was to compare the efficacy and tolerability of venlafaxine extended release (ER) with placebo in treating panic disorder. Secondary objectives included comparing paroxetine with venlafaxine ER and placebo.Outpatients aged ≥18 years (placebo, n = 157; venlafaxine ER 75 mg, n = 156; venlafaxine ER 225 mg, n = 160; paroxetine, n = 151), with a primary diagnosis of panic disorder (±agoraphobia) based on the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) criteria for ≥3 months were randomly assigned to receive venlafaxine ER (titrated to 75 mg/day or 225 mg/day), paroxetine (titrated to 40 mg/day), or placebo for 12 weeks. The primary efficacy measure was the percentage of patients free of full-symptom panic attacks (≥ four symptoms) at endpoint. Key secondary outcomes included the Panic Disorder Severity Scale (PDSS) mean score change and response.At endpoint, all active treatment groups showed a significantly (P < 0.01) greater proportion of patients free of full-symptom panic attacks, compared with placebo, and were superior (P < 0.05) on most secondary measures. The venlafaxine ER 225 mg group had significantly (P < 0.05) greater mean PDSS score improvement than the paroxetine group (−12.58 vs −11.87) and a significantly higher proportion of patients free of full symptom panic attacks (70.0 vs 58.3%). Both drugs were generally well tolerated.Venlafaxine ER 75 mg/days and 225 mg/days and paroxetine 40 mg/day were both well tolerated and effective for short-term treatment of panic disorder.

Keywords: Venlafaxine; Paroxetine; Panic disorder; Agoraphobia; Pharmacotherapy; Panic attack

Defensive-like behaviors induced by ultrasound: further pharmacological characterization in Lister-hooded rats by Laurent B. Nicolas; Steffen Klein; Eric P. Prinssen (pp. 243-252).
In rats, dorsal periaqueductal gray (dPAG) stimulation elicits escape behavior that is thought to be related to fear and panic. A noninvasive technique—exposure to ultrasound—has been reported to stimulate the dPAG and induce escape followed by freezing in Lister-hooded (LH) rats.Further characterize pharmacologically the ultrasound-induced defensive behaviors test with anxiolytics acting via different mechanisms.LH rats, treated with clinically validated anxiolytics, putative anxiolytics, or compounds devoid of anxiolytic properties, were exposed to ultrasound. Baseline locomotion before and duration of escape and freezing behaviors during ultrasound were measured.The low-potency benzodiazepine receptor agonists, diazepam and chlordiazepoxide, selectively reduced escape compared to baseline locomotor activity. The high-potency agonist alprazolam, the mGlu2/3 receptor agonist LY 354740, and the mGlu5 receptor antagonist MTEP reduced escape but did not show such a separation. The voltage-dependent calcium channel inhibitors, pregabalin and gabapentin, selectively reduced escape. The nociceptin OFQ peptide receptor agonist Ro 64-6198 did not affect escape but reduced freezing, an effect that was not produced by any of the other compounds. Buspirone and morphine did not affect escape. As expected, haloperidol reduced escape in a nonselective manner.The present data demonstrate that ultrasound-induced defensive behaviors in LH rats can be independently modulated by anxiolytics of different classes. In particular, ultrasound-induced escape shows sensitivity to the majority of acute therapeutics effective in panic disorder, although sensitivity to compounds with slow onset of action (e.g., antidepressants) remains to be demonstrated.

Keywords: Ultrasound; Periaqueductal gray; Panic; Fear; Anxiety; Defensive behaviors; Anxiolytics; Rats

Appetitive nature of drug cues re-confirmed with physiological measures and the potential role of stage of change by Jared P. Dempsey; Lee M. Cohen; Valerie L. Hobson; Patrick K. Randall (pp. 253-260).
Smokers report pleasant reactions to viewing cigarettes, suggesting that smoking cues may be appetitive in nature. Two studies have investigated this hypothesis through physiological assessment. The first study found that smoking cues were physiologically appetitive in nature, with dampened startle response to smoking pictures in comparison to neutral pictures. The second found that smoking pictures did not modulate the startle response, suggesting such cues may not be physiologically appetitive.The goal of the present study was to further investigate how participants’ motivation to quit smoking might modulate responses to smoking cues.Twenty-two nicotine-dependent smokers viewed standardized pleasant, unpleasant, neutral, and smoking pictures. Eleven of the subjects reported no intent to quit (precontemplators) and 11 reported planning to quit within the next 6 months (contemplators). Acoustic startle probes were randomly administered while subjects viewed the pictures, and eyeblink startle magnitude was measured with electromyography (EMG).As a whole, participants exhibited dampened startle responses during smoking pictures, relative to unpleasant pictures. Precontemplators showed robust startle inhibition to smoking pictures, in comparison to both neutral and unpleasant pictures. Contemplators, however, showed blunted unpleasant picture augmentation and a lack of startle inhibition for pleasant pictures.These findings are consistent with the idea that smoking pictures are appetitive in nature. Furthermore, they suggest that smokers at a later stage of change may exhibit a lesser response.

Keywords: Smoking cues; Affective modulation; Acoustic startle reflex; Nicotine; Stage of change; Transtheoretical; Drug cue

Emotion-induced retrograde amnesia varies as a function of noradrenergic-glucocorticoid activity by René Hurlemann; Andreas Matusch; Barbara Hawellek; Dietrich Klingmuller; Heike Kolsch; Wolfgang Maier; Raymond J. Dolan (pp. 261-269).
Privileged episodic encoding of an aversive event often comes at a cost of neutral events flanking the aversive event, resulting in decreased episodic memory for these neutral events. This peri-emotional amnesia is amygdala-dependent and varies as a function of norepinephrine activity. However, less is known about the amnesiogenic potential of cortisol.We used a strategy of pharmacologically potentiating cortisol and norepinephrine activity to probe the putative neurochemical substrates of peri-emotional amnesia.Fifty-four healthy individuals participated in a randomized double-blind placebo-controlled study. Within the experimental context of an established peri-emotional amnesia paradigm, we tested the amnesiogenic potential of hydrocortisone (30 mg p.o.) in the presence or absence of the norepinephrine-reuptake inhibitor reboxetine (4 mg p.o.).Under dual challenge conditions, we observed a linear dose–response relationship in the magnitude and duration of emotion-induced retrograde amnesia.Our results are consistent with a phenotypic expression of retrograde amnesia varying as a function of norepinephrine and cortisol coactivation during episodic encoding of aversive events. Our study demonstrates that the adverse cognitive and behavioral sequelae of aversive emotion can be experimentally modeled by a pharmacological manipulation of its putative neurochemical substrates.

Keywords: Emotion; Amnesia; Memory; Stress; Cortisol; Norepinephrine; Reboxetine

Intracerebroventricular administration of nitric oxide-sensitive guanylyl cyclase inhibitors induces catalepsy in mice by M. B. Echeverry; M. L. Salgado; F. R. Ferreira; C. A. da-Silva; E. A. Del Bel (pp. 271-278).
Catalepsy is a preclinical test that predicts extrapyramidal symptoms in humans. It models symptoms of acute extrapyramidal side effects induced at the beginning of antipsychotic treatment. Nitric oxide (NO) plays a role in a series of neurobiological functions underlying behavior. For example, inhibition of NO synthesis disrupts rodent exploratory behavior and induces catalepsy. Although several effects mediated by NO involve the activation of soluble guanylyl cyclase (sGC), the transduction mechanism of the catalepsy-inducing effect of NO has not yet been investigated.The study was designed to test if intracerebroventricular (i.c.v.) microinjection of NO-sensitive inhibitors of sGC (NO-sGC) induces catalepsy in mice similar to that induced by NO synthase (NOS) inhibitors. Exploratory behavior was tested in the open field. In addition, the effects of a NOS inhibitor on oxidative metabolites of NO were measured in the striatum.Drug effects were examined in the hanging-bar test after the following i.c.v. treatments: oxadiazolo-quinoxalin (ODQ, 30–300 nmol) or methylene blue (MB, 3–100 nmol), selective and nonselective sGC inhibitors, respectively, or 7-nitroindazole (7-NI, 3–90 nmol) and G-nitro-l-arginine methyl ester (l-NAME, 3–90 nmol), selective and nonselective neuronal NOS inhibitors. To test if the effects were related to interference with the NO system, additional groups received 7-NI (30 nmol), ODQ (100 nmol), or L-NAME (90 nmol) preceded by l-arginine (l-arg, 30–100 nmol, i.c.v. 30 min before). A possible interference of ODQ and 7-NI on exploratory behavior was tested in an open field. The concentration of nitrites and nitrates (NO x ) in striatum homogenates was measured by the Griess reaction.Both NO-sGC and NOS inhibitors induced catalepsy in mice that lasted for at least 2 h. The range of effective doses of these drugs, however, was limited, and the dose–effect curves had an inverted U shape. The cataleptic effect induced by l-NAME was inversely correlated with NO x products in the striatum. The cataleptic effect of 7-NI and ODQ was prevented by pretreatment with l-arginine. No drug changed exploratory behavior in the open field.This study showed that pharmacological disruption of the endogenous NO-sGC signaling in the central nervous system induces long-lasting catalepsy in mice. Moreover, the cataleptic effect of NOS inhibition correlates with the decrease in NO x products formation in the striatum. The results give further support to the hypothesis that NO plays a role in motor behavior control mediated, at least in part, by cyclic guanosine monophosphate production in the striatum.

Keywords: Nitric oxide; Catalepsy; L-arginine; 7-nitroindazole; l-NAME; ODQ; Intracerebroventricular; Methyl blue; Open-field test; Nitrate; Nitrite; Nitrogen oxides

Effect of impulsivity on craving and behavioral reactivity to smoking cues by Neal Doran; Bonnie Spring; Dennis McChargue (pp. 279-288).
Nearly 25% of American adults remain regular smokers. Current smokers may be especially likely to possess characteristics that impair their ability to quit, such as impulsivity. Impulsive individuals may be overly prone to smoke because they are particularly drawn to rewarding stimuli and related cues. The aim of this study was to test the hypothesis that more impulsive smokers are more responsive to cigarette cues than other smokers.In a repeated measures design, 60 euthymic, adult smokers (50% female) were exposed to a smoking cue and a neutral cue in two experimental sessions. Cue reactivity was operationalized as changes in cigarette craving and preference for immediate vs delayed smoking after cue exposure.Impulsivity predicted a heightened craving response to both cues but particularly the smoking cue (t [161] = 3.21, p = 0.002). Smokers with high levels of impulsivity exhibited a greater preference for immediate rewards over larger, delayed rewards in terms of both hypothetical (t [58] = 5.99, p = 0.001) and actual (z = 3.02, p = 0.003) rewards.These data suggest that increased reactivity to environmental smoking cues contributes to the link between impulsivity and smoking.

Keywords: Nicotine; Disinhibition; Reward

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