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Nicotine withdrawal alters neural responses to psychosocial stress.

ABSTRACT: Psychosocial stress is considered to be an important mechanism underlying smoking behavior and relapse. Thus, understanding the effects of acute nicotine withdrawal on responses to stress is important to intervene to prevent stress-induced relapse. The current study investigated the neural correlates of psychosocial stress during acute nicotine withdrawal in chronic smokers.Thirty-nine treatment-seeking smokers were randomized to one of two conditions (abstinent 24 h (n?=?21) or smoking as usual (n?=?18)). They were then exposed to the Montreal Imaging Stress Task (MIST), a psychosocial stress task consisting of difficult mental arithmetic problems while receiving negative performance feedback while undergoing functional magnetic resonance imaging (fMRI).Subjective measures of stress increased following the MIST, compared to baseline. Whole brain between-group analysis identified significant activation clusters in four regions for the stress induction minus control contrast: inferior frontal gyrus (IFG), anterior/para cingulate cortex (ACC), precuneus, and supramarginal gyrus (SMG). In all regions, the deprived group showed significantly greater activation compared to the non-deprived group. No significant correlations were found between subjective stress and BOLD signal activation (ps?>?0.07).This study provides new evidence that brain regions previously shown to be predictive of relapse, such as the precuneus and IFG, display heightened neural responses to stress during nicotine deprivation. These data identify the brain regions that may be associated with withdrawal-related stress responses. Increased stress-related activation during nicotine withdrawal may identify those most vulnerable to relapse and represent a target for novel pharmacological intervention.

SUBMITTER: Ashare RL

PROVIDER: S-EPMC4907902 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Nicotine withdrawal alters neural responses to psychosocial stress.

Ashare Rebecca L RL Lerman Caryn C Cao Wen W Falcone Mary M Bernardo Leah L Ruparel Kosha K Hopson Ryan R Gur Ruben R Pruessner Jens C JC Loughead James J

Psychopharmacology 20160418 13

<h4>Introduction</h4>Psychosocial stress is considered to be an important mechanism underlying smoking behavior and relapse. Thus, understanding the effects of acute nicotine withdrawal on responses to stress is important to intervene to prevent stress-induced relapse. The current study investigated the neural correlates of psychosocial stress during acute nicotine withdrawal in chronic smokers.<h4>Methods</h4>Thirty-nine treatment-seeking smokers were randomized to one of two conditions (abstin ...[more]

PMID: 27087432

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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:BackgroundNicotine withdrawal syndrome is a major clinical problem. Animal models with sufficient predictive validity to support translation of pre-clinical findings to clinical research are lacking.AimsWe evaluated the behavioural and neurochemical alterations in zebrafish induced by short- and long-term nicotine withdrawal.MethodsZebrafish were exposed to 1 mg/L nicotine for 2 weeks. Dependence was determined using behavioural analysis following mecamylamine-induced withdrawal, and brain nicotinic receptor binding studies. Separate groups of nicotine-exposed and control fish were assessed for anxiety-like behaviours, anhedonia and memory deficits following 2-60 days spontaneous withdrawal. Gene expression analysis using whole brain samples from nicotine-treated and control fish was performed at 7 and 60 days after the last drug exposure. Tyrosine hydroxylase (TH) immunoreactivity in pretectum was also analysed.ResultsMecamylamine-precipitated withdrawal nicotine-exposed fish showed increased anxiety-like behaviour as evidenced by increased freezing and decreased exploration. 3H-Epibatidine labeled heteromeric nicotinic acethylcholine receptors (nAChR) significantly increased after 2 weeks of nicotine exposure while 125I-αBungarotoxin labeled homomeric nAChR remained unchanged. Spontaneous nicotine withdrawal elicited anxiety-like behaviour (increased bottom dwelling), reduced motivation in terms of no preference for the enriched side in a place preference test starting from Day 7 after withdrawal and a progressive decrease of memory attention (lowering discrimination index). Behavioural differences were associated with brain gene expression changes: nicotine withdrawn animals showed decreased expression of chrna 4 and chrna7 after 60 days, and of htr2a from 7 to 60 days.The expression of c-Fos was significantly increased at 7 days. Finally, Tyrosine hydroxylase (TH) immunoreactivity increased in dorsal parvocellular pretectal nucleus, but not in periventricular nucleus of posterior tuberculum nor in optic tectum, at 60 days after withdrawal.ConclusionsOur findings show that nicotine withdrawal induced anxiety-like behaviour, cognitive alterations, gene expression changes and increase in pretectal TH expression, similar to those observed in humans and rodent models.

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Nicotine withdrawal alters neural responses to psychosocial stress.

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Nicotine withdrawal alters neural responses to psychosocial stress.

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