Impulsivity In Humans Research Articles

Habitual intake of fat and sugar is associated with poorer memory and greater impulsivity in humans.

The vicious cycle model of obesity suggests that repeated habitual intake of a diet high in fat and sugar (HFS) results in impairment in hippocampal function which in turn increases impulsive behaviours, making it harder to resist unhealthy diet choices. Evidence from studies with rodents consistently show switching to a HFS diet impairs performance on hippocampally-sensitive memory tasks. The limited literature in humans also suggest impaired memory and increased impulsivity related to higher habitual HFS intake. However, these changes in memory and impulsivity have been looked at independently. To investigate how these effects are inter-related, three experiments were conducted where relative HFS intake was related to measures of memory and impulsivity. In Experiment 1 (90 female participants), HFS was associated with higher scores on the Everyday Memory Questionnaire-revised (EMQ), and higher scores on the total, Attention (BISatt) and Motor (BISmot) sub-scales of the Barratt Impulsiveness Scale (BIS11). Experiment 2 (84 women and 35 men), replicated the association between HFS and EMQ, and also found HFS related to poorer performance on the hippocampally-sensitive 4 mountain (4MT) memory task. The association between HFS intake and the BISatt replicated, but there were no significant associations with other BIS11 measures or delay-discounting for monetary rewards. Experiment 3 (199 women and 87 men) replicated the associations between DFS and 4MT and EMQ, and also found an association with overall recall, but not response inhibition, from a Remembering Causes Forgetting task: HFS was also significantly associated with BIS total, BISatt and BISmot. In all three studies these associations remained when potential confounds (BMI, age, gender, hunger state, restrained and disinhibited eating) were controlled for. Mediation analysis found that the effect of HFS on memory at least part mediated the relationship between HFS and impulsivity in Experiments 1 and 3, but not 2. Overall these data provide some support for the vicious cycle model, but also suggest that trait impulsivity may be a risk factor for poor dietary choice.

Unraveling the Contribution of Serotonergic Polymorphisms, Prefrontal Alpha Asymmetry, and Individual Alpha Peak Frequency to the Emotion-Related Impulsivity Endophenotype

The unique contribution of the serotonin transporter-linked polymorphic region (5-HTTLPR), intronic region 2 (STin2), and monoamine oxidase A (MAO-A) genes to individual differences in personality traits has been widely explored, and research has shown that certain forms of these polymorphisms relate to impulsivity and impulsivity-related disorders. Humans showing these traits are also described as having an asymmetrical prefrontal cortical activity when compared to others. In this explorative study, we examine the relationship between serotonergic neurotransmission polymorphisms, cortical activity features (prefrontal alpha asymmetry, individual alpha peak frequency [iAPF]), emotion-related and non-emotion-related impulsivity in humans. 5-HTTLPR, MAO-A, and STin2 polymorphisms were assessed in blood taken from 91 participants with high emotion-related impulsivity levels. Sixty-seven participants completed resting electroencephalography and a more comprehensive impulsivity index. In univariate analyses, iAPF correlated with both forms of emotion-related impulsivity. In multiple linear regression models, 5-HTTLPR polymorphism (model 1, adj. R2 = 15.2%) and iAPF were significant interacting predictors of emotion-related impulsivity, explaining a large share of the results’ variance (model 2, adj. R2 = 21.2%). Carriers of the low transcriptional activity 5-HTTPLR and MAO-A phenotypes obtained higher emotion-related impulsivity scores than others did. No significant results were detected for non-emotion-related impulsivity or for a form of emotion-related impulsivity involving cognitive/motivational reactivity to emotion. Our findings support an endophenotypic approach to impulsivity, showing that tri-allelic 5-HTTLPR polymorphism, iAPF, and their interaction are relevant predictors of one form of emotion-related impulsivity.

From skinner box to daily life: Sign-tracker phenotype co-segregates with impulsivity, compulsivity, and addiction tendencies in humans

Pavlovian conditioning holds the potential to incentivize environmental cues, leading to approach behavior toward them, even outside our awareness. Animal models suggest that this is particularly true for the so-called sign-tracker (ST) phenotype, which is considered to reflect a predisposition toward developing addiction-related behaviours. Despite its potential clinical relevance, few studies have demonstrated the translational validity of this model, likely due to difficulties in studying Pavlovian processes in humans. To fill this gap, we combined an ecological momentary assessment with ambulatory peripheral autonomic monitoring to test the hypothesis that traits associated with ST in preclinical studies would be associated with attribution of high incentive salience to reward-related cues. Several times for 2 days, participants were asked to rate the attractiveness of several preselected ecological rewards (e.g., coffee) and the preceding cues (the smell of coffee) while their electrocardiogram was recorded. While no absolute difference in subjective and physiological measures of motivational approach to daily cues compared with rewards emerged, individuals with high levels of impulsivity, obsessive-compulsive, and addiction-prone behaviors rated as more attractive and showed a greater increase in sympathetic arousal to cues versus rewards. The opposite pattern emerged for those with low levels in those dispositional traits, who responded more (both subjectively and physiologically) to rewards compared with their preceding cues. This study represents an attempt to answer the call to parcel complex behaviors into smaller constructs, improving the early detection of those who are vulnerable to develop psychopathological disorders, particularly in the domain of impulse control such as addiction.

Testosterona and suicide

IntroductionTestosterone is an anabolic androgenic steroid hormone involved in brain development, reproduction, and social behavior. Several studies have shown that testosterone can cause impulsivity in humans. This impulsivity could modify the mood and increase the risk of suicidal behaviour.ObjectivesTestosterone is an anabolic androgenic steroid hormone involved in brain development, reproduction, and social behavior. Several studies have shown that testosterone can cause impulsivity in humans. This impulsivity could modify the mood and increase the risk of suicidal behaviour.MethodsClinical case and literature review.ResultsA 33-years male (biological female), single, gypsy ethnicity, with an 11-years daughter. Psychiatric history of one admission in a hospitalization unit. Diagnosed of depressive disorder and personality disorder NOS. Intermittent follow-up in Mental Health consultations. 8 years later, he consulted due to gender dysphoria. He refered not to be feeling identified with his body for a long time. He rejected his sexual characteristics. After his mental evaluation, he was refered to Endocrinology Service. He had been prescribed with testosterone. Three days after starting the treatment, he maked anattempt of suicide with medication. The patient had not presented previous suicide attempts or ideation. With the withdrawal of the testosterone, the suicidal behaviour dissapeared.ConclusionsDue to the association of testosterone and suicidal behavoiur, we consider that is important to pay attention to people who have just started the androgenic treatment in order to avoid a high risk of suicide. In the same way, we should focus on evaluating the hostility, impulsivity and irritability in patients strongly related to suicidal behaviour.DisclosureNo significant relationships.

Pain-induced Impulsivity and Its Reduction with Amphetamine in Rats

Pain is known to produce various cognitive changes, including increased impulsivity in humans and animals. Increases in impulsivity may facilitate the development of psychiatric conditions such as substance use disorders and anxiety disorders. We have previously shown that Complete Freund's Adjuvant (CFA)-induced pain increases impulsivity in rats. Amphetamine is a central nervous system stimulant used to treat impulse control disorders by increasing monoaminergic activity in the brain. This study aimed to determine whether amphetamine can reduce pain-induced impulsivity and nociception in rats. Pain-induced impulsivity was assessed using a delay discounting task in male and female rats. Initial baseline tests were employed to screen for trait impulsivity and identify low and high impulsive rats. After intraplantar CFA injection, daily saline or amphetamine (0.25, 0.5, or 1.0 mg/kg) was given, and impulsivity was assessed over sixteen days. Animals were also examined for potential antinociceptive effects of amphetamine on CFA-induced tactile allodynia. CFA treatment increased impulsivity in high impulsive rats more than low impulsive rats. Repeated amphetamine administration blocked pain-induced impulsivity in a dose manner. Amphetamine began to block impulsivity after six daily injections. CFA-induced mechanical allodynia was not reduced by amphetamine. Our results show amphetamine's propensity to prevent pain-induced impulsivity, independent of treating nociception. While pain-induced cognitive deficits may proliferate from pain states, their treatment and continued expression may be independent of pain sensation.

The Effects of Mild Traumatic Brain Injury (mTBI) on Serotonergic Gene Expression

Traumatic brain injury (TBI) is a risk factor for suicide. Approximately 1.7 million TBIs occur each year and new TBI cases in the U.S. military have more than doubled in the last 5 years. The majority of military TBIs are mild in severity and can lead to chronic symptoms including, impulsivity, emotional instability, and impaired inhibition. Impulsivity is one of the most frequent behavioral changes seen following mTBI and involves poor response inhibition and/or poor decision making. Also, impulsivity is a key risk factor for suicide. The serotonergic system is an important modulator of impulsivity and, thus, a molecular target for understanding the behavioral changes in impulsivity that occur following mTBI. One major source of serotonin in the brain is the raphe nuclei in the pons. The serotonergic neurons in the raphe nuclei project to the prefrontal cortex, frontal cortex and hippocampus and are involved in many cognitive processes related to impulsivity and suicidality. In addition, both animal and human research indicates that the brainstem is affected in mTBI, particularly, in the lateral fluid percussion model utilized in this study. This provides additional support for the notion that mTBI may lead to dysfunction of the serotonin producing raphe nuclei located in the brain stem. In this study, changes in serotonergic gene expression in the raphe nuclei and target regions including the prefrontal cortex, frontal cortex and hippocampus were assessed using qRT‐PCR. Rats sustained a single mTBI induced using the lateral fluid percussion model and were sacrificed three months following injury. Brains were extracted, flash frozen, sectioned at 300um and tissue for the raphe nuclei and target regions was collected using a 1.5 mm tissue punch. RNA was extracted from the tissue punches, reverse transcribed into cDNA and qRT‐PCR was performed. The hypothesis states that mTBI leads to altered expression of serotonin related genes in the raphe nuclei and/or raphe nuclei target regions including the prefrontal cortex, frontal cortex, and hippocampus. Results show altered expression levels of tryptophan hydroxylase and serotonin transporter genes in both the medial raphe and dorsal raphe nuclei in mTBI rats compared to SHAM control rats. Changes in expression levels of the 5HT1A and 5HT2A receptor genes were also seen in the frontal cortex, prefrontal cortex, and ventral hippocampus. The current study serves to provide evidence for a link between TBI and altered serotonin levels to better understand the molecular mechanisms underlying impulsivity and suicidality in humans following TBI.

Can impulsivity evolve in response to childhood environmental harshness?

Previous studies have suggested that human impulsivity is an adaptive response to childhood environmental harshness: individuals from families of low socioeconomic status (SES) tend to be more impulsive. However, no studies have tested the evolvability of this reaction norm. This study examined whether (a) impulsivity is associated with higher fitness among individuals from low SES families, while (b) it is associated with lower fitness among individuals from high SES families. We assessed three indices of impulsivity (temporal discounting, risk taking and fast/slow life history strategy), childhood SES and five proxy indices of fitness (number of children, lifelong singlehood, annual household income, subjective SES and life satisfaction) of 692 middle-aged participants (40-45 years old). None of the results supported the evolvability of the impulsivity reaction norm, although low childhood SES was associated with lower fitness on every proxy measure. Impulsivity (operationalised as the fast life history strategy) was associated with lower fitness regardless of childhood SES.

Assessing Impulsivity in Humans and Rodents: Taking the Translational Road

Impulsivity is a multidimensional construct encompassing domains of behavioral inhibition as well as of decision making. It is often adaptive and associated with fast responses, being in that sense physiological. However, abnormal manifestations of impulsive behavior can be observed in contexts of drug abuse and attention-deficit/hyperactivity disorder (ADHD), among others. A number of tools have therefore been devised to assess the different facets of impulsivity in both normal and pathological contexts. In this narrative review, we systematize behavioral and self-reported measures of impulsivity and critically discuss their constructs and limitations, establishing a parallel between assessments in humans and rodents. The first rely on paradigms that are typically designed to assess a specific dimension of impulsivity, within either impulsive action (inability to suppress a prepotent action) or impulsive choice, which implies a decision that weighs the costs and benefits of the options. On the other hand, self-reported measures are performed through questionnaires, allowing assessment of impulsivity dimensions that would be difficult to mimic in an experimental setting (e.g., positive/negative urgency and lack of premeditation) and which are therefore difficult (if not impossible) to measure in rodents.

The acute and repeated effects of cigarette smoking and smoking-related cues on impulsivity.

Impulsivity may be a risk factor that increases vulnerability to nicotine dependence. However, nicotine exposure itself may directly increase impulsivity. This is a secondary analysis of the first study in a controlled laboratory setting, which assessed the effects of nicotine administration (acute and repeated) and exposure to smoking cues on behavioural impulsivity in humans (ClinicalTrials.gov Identifier: NCT01395797). Twenty-seven smokers completed three tasks to assess behavioural impulsivity (the Immediate Memory Task and the Delayed Memory Task assessing response initiation, and the GoStop Task assessing response inhibition) following: (i) 4 days of cigarette smoking (nicotinised or denicotinised cigarette); (ii) acute cigarette smoking (nicotinised); and (iii) exposure to smoking-related cues. Four days of nicotinised cigarette smoking (vs. denicotinised) did not significantly increase Immediate Memory Task, Delayed Memory Task and GoStop scores. However, acute cigarette smoking increased GoStop impulsivity, but only following 4 days of smoking nicotinised cigarettes (P < 0.05). Exposure to smoking-related cues had no statistically significant effect on impulsivity. Our results suggest that repeated nicotine exposure may sensitise subsequent acute nicotine effects on behavioural impulsivity in heavy smokers.

Medial forebrain bundle structure is linked to human impulsivity.

Comparative research indicates that projections from midbrain dopamine nuclei [including the ventral tegmental area (VTA)] to the ventral striatum [including the nucleus accumbens (NAcc)] critically support motivated behavior. Using diffusion-weighted imaging and probabilistic tractography in humans, we characterized the trajectory and structure of two tracts connecting the VTA and NAcc, as well as others connecting the substantia nigra and dorsal striatum. Decreased structural coherence of an inferior VTA-NAcc tract was primarily and replicably associated with increased trait impulsivity and also distinguished individuals with a stimulant use disorder from healthy controls. These findings suggest that decreased coherence of the inferior VTA-NAcc tract is associated with increased impulsivity in humans and identify a previously uncharacterized structural target for diagnosing disorders marked by impulsivity.

Dietary intake of tryptophan tied emotion-related impulsivity in humans.

Emotion-related impulsivity, defined as the tendency to say or do things that one later regret during periods of heightened emotion, has been tied to a broad range of psychopathologies. Previous work has suggested that emotion-related impulsivity is tied to an impaired function of the serotonergic system. Central serotonin synthesis relies on the intake of the essential amino acid, tryptophan and its ability to pass through the blood brain barrier. Objective: The aim of this study was to determine the association between emotion-related impulsivity and tryptophan intake. Methods: Undergraduate participants (N=25, 16 women, 9 men) completed a self-rated measure of impulsivity (Three Factor Impulsivity Index, TFI) and daily logs of their food intake and exercise. These data were coded using the software NutriNote to evaluate intakes of tryptophan, large neutral amino acids, vitamins B6/B12, and exercise. Results: Correlational analyses indicated that higher tryptophan intake was associated with significantly lower scores on two out of three subscales of the TFI, Pervasive Influence of Feelings scores r=-.502, p<.010, and (lack-of) Follow-Through scores, r=-.407, p<.050. Conclusion: Findings provide further evidence that emotion-related impulsivity is correlated to serotonergic indices, even when considering only food habits. It also suggests the need for more research on whether tryptophan supplements might be beneficial for impulsive persons suffering from a psychological disorder.

Waiting impulsivity during reward seeking increases adult hippocampal neurogenesis in mice

Impulsivity is defined as a predisposition toward rapid, unplanned reactions in response to internal or external stimuli, often yielding negative consequences. Accordingly, impulsivity is considered a significant risk factor for developing addictive behaviors. The hippocampus is involved in regulating behavioral adaptability and learned behaviors. Consequently, abnormal hippocampal function has been demonstrated to contribute to impulsive and addictive behaviors. Furthermore, differential reinforcement of low rates of behavior (DRL) has shown that the hippocampus is implicated in reward acquisition and impulsivity in humans and rodent models. We have previously shown that impulsive behavior potentiates hippocampal neuroblast proliferation. However, the fate of these precursor cells produced during impulsive reward seeking remains unknown. Here, we demonstrate that DRL-mediated impulsive reward seeking with the 2-choice reaction time task (2-CRTT) increases the number of BrdU labeled cells in the dentate gyrus region of the hippocampus. Importantly, our results also show a significant increase in BrdU+ and NeuN+ colocalized mature newborn neurons in mice exhibiting impulsivity compared to non-impulsive control mice. These results suggest that operant reward seeking during unpredictable schedules of reinforcement contributes to adult hippocampal neurogenesis.

Serotonin Receptor 1A Variation Is Associated with Anxiety and Agonistic Behavior in Chimpanzees.

Serotonin is a neurotransmitter that plays an important role in regulating behavior and personality in humans and other mammals. Polymorphisms in genes coding for the serotonin receptor subtype 1A (HTR1A), the serotonin transporter (SLC6A4), and the serotonin degrading enzyme monoamine oxidase A (MAOA) are associated with anxiety, impulsivity, and neurotic personality in humans. In primates, previous research has largely focused on SLC6A4 and MAOA, with few studies investigating the role of HTR1A polymorphic variation on behavior. Here, we examined variation in the coding region of HTR1A across apes, and genotyped polymorphic coding variation in a sample of 214 chimpanzees with matched measures of personality and behavior. We found evidence for positive selection at three amino acid substitution sites, one in chimpanzees-bonobos (Thr26Ser), one in humans (Phe33Val), and one in orangutans (Ala274Gly). Investigation of the HTR1A coding region in chimpanzees revealed a polymorphic site, where a C/A single nucleotide polymorphism changes a proline to a glutamine in the amino acid sequence (Pro248Gln). The substitution is located in the third intracellular loop of the receptor, a region important for serotonin signal transduction. The derived variant is the major allele in this population (frequency 0.67), and is associated with a reduction in anxiety, decreased rates of male agonistic behavior, and an increase in socio-positive behavior. These results are the first evidence that the HTR1A gene may be involved in regulating social behavior in chimpanzees and encourage further systematic investigation of polymorphic variation in other primate populations with corresponding data on behavior.

Hunger and socioeconomic background additively predict impulsivity in humans

Impulsivity refers to the valuation of future rewards relative to immediate ones. From an evolutionary perspective, we should expect impulsivity to be sensitive to the current state of the organism (for example, hunger), and also its long-term developmental history. There is evidence that both current hunger and childhood socioeconomic deprivation are individually associated with impulsivity, but it is not known how these combine. For example, acute hunger might over-ride social gradients in baseline impulsivity, or alternatively, individuals who have experienced greater deprivation might respond more strongly to acute hunger. We aimed to investigate whether hunger and childhood socioeconomic deprivation act additively or interactively in three studies utilising delay discounting tasks. Childhood socioeconomic deprivation was measured using childhood postcode and a self-report measure. In two studies hunger was experimentally manipulated (n = 95 & n = 93 respectively), and in the third we simply measured natural variation. We employed a standard hypothetical delay discounting task in two studies, and a behavioural task with experienced delays in the third (n = 330). Although the individual studies varied in which predictors were statistically significant, when we meta-analysed them, a clear pattern emerged. Hunger predicted greater impulsivity; childhood socioeconomic deprivation predicted greater impulsivity; and these two effects were additive rather than interactive.

No Evidence for the Watching-Eyes Effect on Human Impulsivity.

People often become more altruistic when they think or feel that someone is watching them. Known as the “watching-eyes effect,” this is argued to be caused by the motivation to gain and maintain a positive social reputation as an altruistic individual (the “reputation seeking” mechanism). However, an alternative mechanism underlying the watching-eyes effect could be that people suppress their impulsive tendency to pursue benefit rather than increase their altruism, and this may lead to apparent increases in altruistic tendencies. This “suppressing impulsivity” mechanism is considered intrapersonal rather than socially mediated which is associated with “reputation seeking.” We examined whether the suppressing impulsivity mechanism would be associated with the watching-eyes effect by measuring participants’ impulsivity in the presence of watching-eyes stimuli. In a controlled experiment, we presented life-size pictures of human faces with a direct gaze on a monitor in front of participants taking part in a time-discounting task. Two types of faces, “in-group” (faces of participants’ classmates) and “out-group” (unfamiliar faces) were presented to examine the effect of social attribution. We used a flower picture as a control stimulus. In the time-discounting task, participants chose one of two options: a small amount of money that they could get immediately or a larger amount of money that they could get after a given time interval. The results showed no significant difference in participants’ time-discount rate regardless of the types of stimuli presented during the time-discount task. A post-task questionnaire confirmed that the participants were aware of the presented stimuli and revealed that they paid more attention to the in-group stimuli than to the out-group and flower stimuli, though this difference in attentive states had no effect on their impulsivity during the task. These results suggest that suppressing impulsivity is not a plausible mechanism for the watching-eyes effect. The null effect for the difference between the in-group and out-group stimuli also supports this conclusion. Thus, it is plausible that the watching-eyes effect is caused by the human tendency to boost social reputation and can be mediated by the social relationship with others.

Chronic Testosterone Increases Impulsivity and Influences the Transcriptional Activity of the Alpha-2A Adrenergic Receptor Signaling Pathway in Rat Brain

Testosterone is an anabolic androgenic steroid hormone involved in brain development, reproduction, and social behavior. Several studies have shown that testosterone can cause impulsivity in humans, which in turn, is linked with mood-related psychiatric disorders and higher risk of death by suicide. The mechanisms by which testosterone abuse influences impulsivity are unclear. The present study aims to understand how testosterone influences impulsivity in a rodent model both at behavioral and molecular levels. In this study, rats were either only gonadectomized or gonadectomized and injected with supraphysiological doses of testosterone. Their relative impulsivity levels were assessed using the go/no-go task. Serum level of testosterone was measured using ELISA. Transcript levels of alpha-2A adrenergic receptor (Adra2a), G proteins (stimulatory subunit-Gαs [Gnas], inhibitory subunit-Giα [Gnai1 and Gnai2]), and catalytic and regulatory subunits of protein kinase A (PKA) were examined using quantitative PCR (qPCR) in brain areas associated with limbic system (prefrontal cortex (PFC), hippocampus, and amygdala). The testosterone-treated (T) group showed significantly higher level of serum testosterone and displayed a lower go/no-go ratio, indicating greater impulsivity compared to the gonadectomized (GDX) group. The transcript levels Adra2a and Gαs genes and PKA subunits encoded by Prkar1a, Prkar1b, Prkar2a, and Prkaca genes were significantly upregulated in PFC of testosterone treated rats. The expression levels of these genes were not significantly altered in hippocampus. On the other hand, amygdala showed changes only in Gnas and Prkar2a. These results suggest that chronic testosterone influences impulsivity possibly via hyperactive alpha-2A adrenergic receptor-PKA signaling axis, specifically in the PFC.

Frontal brain injury chronically impairs timing behavior in rats

Traumatic brain injury (TBI) affects over 2.8 million people annually, and has been shown to increase motor impulsivity in both humans and animals. However, the root cause of this behavioral disinhibition is not fully understood. The goal of the current study was to evaluate whether timing behavior is disrupted after TBI, which could potentially explain increases in impulsive responding. Twenty-one male three-month old Long-Evans rats were trained on a fixed interval-18 s schedule. Following training, rats were placed on the Peak Interval Procedure, with intermittent peak trials. On peak trials, no behaviors were reinforced and response rates were recorded to determine timing ability. After reaching a stable baseline, rats received bilateral frontal TBI (n = 12) using controlled cortical impact or sham procedures (n = 9). After one week recovery, rats were re-assessed on the Peak Procedure for six weeks. An amphetamine challenge was carried out after behavior reached stable post-injury performance. TBI caused a chronic decrease/acceleration in peak time, increase in response variability, and reduction in response rate. The shifted peak time suggests that altered perception of time may contribute to impairments in response inhibition after TBI. Amphetamine significantly increased response variability, with TBI animals demonstrating greater sensitivity, but did not affect peak time in either group. These data suggest that timing may not be the sole factor explaining impulsive action after TBI given that amphetamine reduced motor impulsivity in prior studies. Further investigations will be needed to dissociate the effects of amphetamine on TBI with regard to timing behavior.

SERT gene polymorphisms are associated with risk-taking behaviour and breeding parameters in wild great tits

Individual differences in coping with potentially dangerous situations are affected by a combination of genetic and environmental factors. How genetic polymorphisms and behavioural variations are related to fitness is unknown. One of the candidate genes affecting a variety of behavioural processes, including impulsivity, anxiety and mood fluctuations in both humans and other vertebrates, is the serotonin transporter gene (SERT/SLC6A). The aim of this study was to assess an association between SERT genotypes and novelty-seeking and risk-taking behaviours as well as breeding parameters of great tits (Parus major) in a natural environment. We associated polymorphisms in the promoter exonic regions of the SERT gene with parental risk-taking-related behaviour and fitness traits. Our results show that: (1) risk-taking behaviour in our great tit population is linked to single nucleotide polymorphisms in the SERT gene exon 3 and exon 8; (2) the genotype-behaviour associations are consistent with the presence of different stressors; and (3) polymorphisms in exon 8 could be associated with fitness-related traits, such as the start of egg-laying and hatching success. We showed for the first time that genetic variability of SERT plays an important role in shaping individual decision-making that affects fitness in a wild population. However, the results are based on one population and on the polymorphisms that are in a single gene. Therefore, replication studies are needed in order to confirm these preliminary results.

Relationship of low doses of alcohol voluntarily consumed during adolescence and early adulthood with subsequent behavioral flexibility.

Previous alcohol use is associated with impaired decision-making and impulsivity in humans, but the relationship between alcohol use and decision-making/impulsivity is unclear. In two experiments, we determined whether chronic intermittent access to alcohol during adolescence and early adulthood would alter or be correlated with performance in a go/no-go reversal task, a devaluation task, or operant extinction. Rats received 6 weeks of chronic intermittent access to 20% alcohol or water from postnatal day 26 to 66 and then behavioral testing was initiated 1.5-2.5 weeks later. We found no evidence that voluntary alcohol consumption altered behavior in either task. However, we found that rats that consumed more alcohol made fewer commission errors in reversal learning compared with rats that drank less. There was no relationship between alcohol consumption and reversal learning omission errors. Alcohol consumption was not correlated with the magnitude of the devaluation effect, but rats that consumed more alcohol showed faster extinction during the devaluation test. Our results suggest that the relationships between behavioral flexibility and alcohol consumption may represent individual differences. Future work will determine the neurobiological and genetic bases of these behavioral differences.

Dissociable effects of cocaine and yohimbine on impulsive action and relapse to cocaine seeking

RationaleA strong association has been demonstrated between various forms of impulsivity and addiction-like behavior in both humans and rats.ObjectivesIn this study, we investigated how impulsive action, as measured in the 5-choice serial reaction time task (5-CSRTT), is affected during various stages of cocaine taking and seeking and by relapse-provoking stimuli in animals that were trained both in an intravenous cocaine self-administration paradigm and in the 5-CSRTT.MethodsRats were concurrently trained in the 5-CSRTT and cocaine self-administration protocol, and subsequently, the effects of cocaine (7.5 mg/kg) and the pharmacological stressor yohimbine (1.25 mg/kg) were tested in both paradigms.ResultsCocaine self-administration (5 h/day) transiently altered impulsive action and increased errors of omission in the 5-CSRTT. Pharmacological challenges with cocaine and yohimbine induced increments in impulsive action and reinstated cocaine-seeking responses within the same animals. Further analyses revealed that the effects of cocaine and yohimbine on impulsive action did not correlate with their effects on reinstatement of cocaine seeking.ConclusionsThese data suggest that although impulsive action and relapse can be pharmacologically modulated in the same direction within individuals, these effects appear not to be directly coupled.