Effects of acute stress on acquisition of nicotine conditioned place preference in adolescent rats: a role for corticotropin-releasing factor 1 receptors

Brielmaier, Jennifer; McDonald, Craig G.; Smith, Robert F.

doi:10.1007/s00213-011-2378-1

Cited by 51 publications

(41 citation statements)

References 79 publications

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“…This effect of stress on motivation has also been shown in animals. Nicotine-naïve rats stressed 24 h earlier acquired place preference at lower doses of nicotine than non-stressed rats (139); the potentiating effect of stress on motivation, but not on acquiring place preference itself, was diminished after pre-treatment with a CRF-1 receptor antagonist. Similarly, stress prior to escalation to regular use in morphine-initiated mice resulted in repeated self-administration of lower dosages irrespective of whether mice preferred low or high dosages prior to stress induction.…”

Section: Effects Of Trauma or Stress On Stages Of The Addiction Cyclementioning

confidence: 99%

Stress Modulates Illness-Course of Substance Use Disorders: A Translational Review

Lijffijt

Swann

2014

Front. Psychiatry

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Childhood trauma and post-childhood chronic/repeated stress could increase the risk of a substance use disorder by affecting five stages of addiction illness-course: (a) initial experimentation with substances; (b) shifting from experimental to regular use; (c) escalation from regular use to abuse or dependence; (d) motivation to quit; and (e) risk of (re-)lapse. We reviewed the human literature on relationships between stress and addiction illness-course. We explored per illness-course stage: (i) whether childhood trauma and post-childhood chronic/repeated stress have comparable effects and (ii) whether effects cut across classes of substances of abuse. We further discuss potential underlying mechanisms by which stressors may affect illness-course stages for which we relied on evidence from studies in animals and humans. Stress and substances of abuse both activate stress and dopaminergic motivation systems, and childhood trauma and post-childhood stressful events are more chronic and occur more frequently in people who use substances. Stressors increase risk to initiate early use potentially by affecting trait-like factors of risk-taking, decision making, and behavioral control. Stressors also accelerate transition to regular use potentially due to prior effects of stress on sensitization of dopaminergic motivation systems, cross-sensitizing with substances of abuse, especially in people with high trait impulsivity who are more prone to sensitization. Finally, stressors increase risk for abuse and dependence, attenuate motivation to quit, and increase relapse risk potentially by intensified sensitization of motivational systems, by a shift from positive to negative reinforcement due to sensitization of the amygdala by corticotropin releasing factor, and by increased sensitization of noradrenergic systems. Stress generally affects addiction illness-course across stressor types and across classes of substances of abuse.

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Section: Effects Of Trauma or Stress On Stages Of The Addiction Cyclementioning

confidence: 99%

Stress Modulates Illness-Course of Substance Use Disorders: A Translational Review

Lijffijt

Swann

2014

Front. Psychiatry

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“…Stressors facilitate the initiation of smoking and animal studies indicate that stressors potentiate the rewarding effects of nicotine via a CRF 1 receptor dependent mechanism. 6,20 Blockade of CRF 1 receptors diminishes nicotine withdrawal-induced anxiety-like behavior. 21 In addition, nicotine withdrawal leads to an increase in CRF in the central nucleus of the amygdala (CeA) and blockade of CRF 1 receptors in this brain site prevents high levels of nicotine intake.…”

Section: Introductionmentioning

confidence: 99%

Sustained AAV-mediated overexpression of CRF in the central amygdala diminishes the depressive-like state associated with nicotine withdrawal

Shan

et al. 2014

Transl Psychiatry

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Smoking cessation leads to a dysphoric state and this increases the risk for relapse. Animal studies indicate that the dysphoric state associated with nicotine withdrawal is at least partly mediated by an increase in corticotropin-releasing factor (CRF) release in the central nucleus of the amygdala (CeA). In the present study, we investigated whether a sustained overexpression of CRF in the CeA affects the dysphoric-like state associated with nicotine withdrawal. To study brain reward function, rats were prepared with intracranial self-stimulation (ICSS) electrodes in the medial forebrain bundle. An adeno-associated virus (AAV, pseudotype 2/5) was used to overexpress CRF or green fluorescent protein (GFP, control) in the CeA and minipumps were used to induce nicotine dependence. The AAV2/5-CRF vector induced a 40% increase in CRF protein and mRNA levels in the CeA. Administration of the nicotinic receptor antagonist mecamylamine (precipitated withdrawal) or nicotine pump removal (spontaneous withdrawal) led to elevations in ICSS thresholds. Elevations in ICSS thresholds are indicative of a dysphoric-like state. The overexpression of CRF did not affect baseline ICSS thresholds but diminished the elevations in ICSS thresholds associated with precipitated and spontaneous nicotine withdrawal. The real-time reverse transcriptase (RT)–PCR analysis showed that the overexpression of CRF led to a decrease in CRF1 mRNA levels and an increase in CRF2 mRNA levels in the CeA. In conclusion, the overexpression of CRF in the CeA diminishes the dysphoric-like state associated with nicotine withdrawal and this might be driven by neuroadaptive changes in CRF1 and CRF2 receptor gene expression.

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“…It is possible here again that our stress exposure/conditioning regimen was not sufficiently stringent to establish a strong association between the FS and odor cue, or to reveal an effect of the odor cue on the expression of sensitization induced by either repeated stress or cocaine. Neither of these explanations seem likely, however, given that robust FS conditioning has been previously shown to occur within a single session [20,21] and that, in our study, the conditioned stressor did selectively potentiate the effect of a cocaine challenge on the expression of sensitization (Fig. 3d).…”

Section: Introductionmentioning

confidence: 51%

Potentiation of the expression of cocaine-induced sensitization by a conditioned stressor

Sasaki

Sivanathan

Hussain

et al. 2015

Behavioural Brain Research

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Effects of acute stress on acquisition of nicotine conditioned place preference in adolescent rats: a role for corticotropin-releasing factor 1 receptors

Abstract: Taken together, the results suggest that during adolescence, nicotine reward is enhanced by recent stressor exposure in a manner that involves signaling at CRF-R1. Information from studies such as this may be used to inform efforts to prevent and treat adolescent nicotine dependence.

Cited by 51 publications

References 79 publications

Stress Modulates Illness-Course of Substance Use Disorders: A Translational Review

Stress Modulates Illness-Course of Substance Use Disorders: A Translational Review

Sustained AAV-mediated overexpression of CRF in the central amygdala diminishes the depressive-like state associated with nicotine withdrawal

Potentiation of the expression of cocaine-induced sensitization by a conditioned stressor

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