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An acute psychosocial stress enhances the neural response to smoking cues.

ABSTRACT: Stress plays an important role in drug addiction. It can trigger relapse in abstinent addicts, and both in the everyday world and in the laboratory, a stressor can induce drug craving. Drug cues, such as the sight of drug, can also trigger subjective craving and relapse, and this effect may be amplified by stress. Underpinning this interaction may be the fact that stress and reward-predicting drug cues act on overlapping brain regions. We exposed 15 smokers undergoing functional magnetic resonance imaging to a psychosocial stressor, the Montreal Imaging Stress Task, followed by drug cues consisting of video clips of smokers. In a separate session similar video clips were shown after a non-stress control task. We observed significantly decreased neural activity during stress in the hippocampus, amygdala, bed nucleus of the stria terminalis, hypothalamus and nucleus accumbens. Following stress there was an increased neural response to drug cues in the medial prefrontal cortex, posterior cingulate cortex, dorsomedial thalamus, medial temporal lobe, caudate nucleus, and primary and association visual areas. These regions are thought to be involved in visual attention and in assigning incentive value to cues. Stress-induced limbic deactivation predicted subsequent neural cue-reactivity. We suggest that stress increases the incentive salience of drug cues.

SUBMITTER: Dagher A

PROVIDER: S-EPMC2754394 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature

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An acute psychosocial stress enhances the neural response to smoking cues.

Dagher Alain A Tannenbaum Beth B Hayashi Takuya T Pruessner Jens C JC McBride Dharma D

Brain research 20090724

Stress plays an important role in drug addiction. It can trigger relapse in abstinent addicts, and both in the everyday world and in the laboratory, a stressor can induce drug craving. Drug cues, such as the sight of drug, can also trigger subjective craving and relapse, and this effect may be amplified by stress. Underpinning this interaction may be the fact that stress and reward-predicting drug cues act on overlapping brain regions. We exposed 15 smokers undergoing functional magnetic resonan ...[more]

PMID: 19632211

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Project description:FMRI Montreal Imaging Stress Tasks (MIST) have been shown to activate endocrine and autonomic stress responses that are mediated by a prefrontal cortex (PFC)-hippocampus-amygdala circuit. However, the stability of the neurobehavioral responses over time and the ability to monitor response to clinical interventions has yet to be validated. The objective of this study was to compare the fMRI and physiologic responses to acute psychosocial stress in healthy volunteers during initial and follow-up visits approximately 13 weeks later, simulating a typical duration of clinical intervention. We hypothesized that responses to stress would remain highly conserved across the 2 visits in the absence of an intervention. 15 healthy volunteers completed a variant of control math task (CMT) and stress math task (SMT) conditions based on MIST. Neural responses were modeled using an event-related design with estimates for math performance and auditory feedback for each task condition. For each visit, measures of stress reactivity included differential fMRI and heart rate (SMT-CMT), as well as salivary alpha-amylase before and after scanning sessions. The results revealed that differential fMRI, as well as increased heart rate and salivary alpha-amylase from before and after scanning remained similar between visits. Intraclass correlation coefficient (ICC) values revealed areas of reliable task-dependent BOLD fMRI signal response across visits for peaks of clusters for the main effect of condition (SMT vs CMT) within dorsal anterior cingulate cortex (ACC), insula, and hippocampus regions during math performance and within subgenual ACC, posterior cingulate cortex, dorsolateral PFC regions during auditory feedback. Given that the neurobehavioral response to acute stress remained highly conserved across visits in the absence of an intervention, this study confirms the utility for MIST for assessing longitudinal changes in controlled trials that can identify underlying neurobiological mechanisms involved in mediating the efficacy of stress-reduction interventions.

Project description:Background:Childhood maltreatment is a strong risk factor for the development of depression in later life. However, the neurobiological mechanisms underlying this vulnerability are not well understood. As depression has been associated with dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis and increased responsiveness to psychosocial stressors, we speculated that childhood maltreatment may lead to lasting alteration of the stress response system, thereby increasing the risk of depression. This study investigated the effects of childhood maltreatment on the stress response in healthy subjects while controlling for psychiatric condition. Methods:Forty-eight healthy young adults (24 females) with childhood maltreatment experience and 48 healthy controls (33 females) without such experience were administered the Montreal Imaging Stress Task during functional magnetic resonance imaging. Childhood maltreatment experience was assessed using the 28-item Childhood Trauma Questionnaire (CTQ). Between-group differences in subjective stress levels, whole brain activations and cortisol levels were assessed. Results:Relative to healthy control subjects, individuals exposed to childhood maltreatment exhibited higher subjective stress and cortisol levels. Neurofunctionally, participants with histories of childhood maltreatment displayed significantly increased activation in the dorsolateral prefrontal cortex (dlPFC), insula and precuneus, and decreased activation in ventromedial prefrontal cortex (vmPFC) relative to healthy controls during the psychosocial stress task. Activations in dlPFC and insula correlated with CTQ scores in the childhood maltreatment group. Conclusion:The results of this study show that childhood maltreatment induces lasting changes in brain function and HPA-axis responsiveness to stress. The observed abnormal activation in the dlPFC, insula and vmPFC and enhanced cortisol response are similar to those seen in individuals with depression. This dysfunction might serve as a diathesis that embeds latent vulnerability to psychiatric disorders, and this mechanism provides evidence supporting the stress sensitization model.

Project description:BackgroundEvidence suggests an increased risk of smoking among single mothers as compared to their cohabitating counterparts. This article examines the role of psychosocial stress in mediating the relationship between single motherhood and smoking.MethodsData were derived from a cross-sectional population based sample of German women (n = 3129) with underage children (0-18 years of age). Perceived stress was measured with 13 items covering socioeconomic as well as family- and parenting-related stressors. According to Baron and Kenny (1986) a series of logistic regression models was applied to investigate the role of psychosocial stress as a mediator on the relationship between single motherhood and smoking.ResultsAbout 44.0% of single mothers smoked daily, whereas only 26.2% of cohabitating mothers did. Single mothers reported more stress related to their economic situation, occupation and family than partnered mothers. Out of the original 13 stressors only 'conflicts with the partner or ex-partner' and 'financial worries' remained significant in explaining single mothers' higher risk of smoking. Against expectation, stress due to household requirements and family demands was associated with lower odds of single mothers' smoking. After controlling for psychosocial stress, the odds ratio of single mothers' moderate smoking (< 20 cig./day) decreased slightly from 1.75 to 1.66 (explained fraction XF = 12.0%) and with respect to heavy smoking (≥ 20 cig./day) more pronounced from 2.56 to 2.01 (XF = 35.3%).ConclusionsIt can be stated that single mothers' heavy more than moderate smoking appeared to be mediated by perceived psychosocial stress. Out of all stressors considered, financial worries were of paramount significance in explaining single mothers' heavy smoking while some family-related stressors rather appeared to keep single mothers from smoking. Overall, a higher stress exposure explains partly but not sufficiently single mothers' increased smoking rates.

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An acute psychosocial stress enhances the neural response to smoking cues.

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An acute psychosocial stress enhances the neural response to smoking cues.

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