Marinelli M, Piazza PV. Interaction between glucocorticoid hormones, stress and psychostimulant drugs. Eur J Neurosci 16: 387-394

INSERM U259, Université de Bordeaux 2, Rue Camille Saint-Saëns, 33077 Bordeaux Cedex, France.
European Journal of Neuroscience (Impact Factor: 3.18). 09/2002; 16(3):387-94. DOI: 10.1046/j.1460-9568.2002.02089.x
Source: PubMed


In this review we summarize data obtained from animal studies showing that glucocorticoid hormones have a facilitatory role on behavioural responses to psychostimulant drugs such as locomotor activity, self-administration and relapse. These behavioural effects of glucocorticoids involve an action on the meso-accumbens dopamine system, one of the major systems mediating the addictive properties of drugs of abuse. The effects of glucocorticoids in the nucleus accumbens are site-specific; these hormones modify dopamine transmission in only the shell of this nucleus without modifying it in the core. Studies with corticosteroid receptor antagonists suggest that the dopaminergic effects of these hormones depend mostly on glucocorticoid, not on mineralocorticoid receptors. These data suggest that an increase in glucocorticoid hormones, through an action on mesolimbic dopamine neurons, could increase vulnerability to drug abuse. We also discuss the implications of this finding with respect to the physiological role of glucocorticoids. It is proposed that an increase in glucocorticoids, by activating the reward pathway, could counteract the aversive effects of stress. During chronic stress, repeated increases in glucocorticoids and dopamine would result in sensitization of the reward system. This sensitized state, which can persist after the end of the stress, would render the subject more responsive to drugs of abuse and consequently more vulnerable to the development of addiction.

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    • "The interactions between addictive drugs and stress appear to involve some of the main components of the hypothalamicpituitary-adrenal (HPA) axis, one of the key systems involved in the stress response. HPA activation is a common feature of all addictive drugs (Armario, 2010), and glucocorticoids have been implicated in the cross-sensitization and enhanced vulnerability to psychostimulant self-administration (Marinelli and Piazza, 2002). Moreover, the corticotropin-releasing hormone (CRH), the main hypothalamic factor regulating the HPA axis, is strongly involved in different aspects of addiction (Zorrilla et al., 2014). "
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    ABSTRACT: There have been numerous studies into the interaction between stress and addictive drugs, yet few have specifically addressed how the organism responds to stress when under the influence of psychostimulants. Thus, we studied the effects of different acute stressors (immobilization, interleukin-1β and forced swimming) in young adult male rats simultaneously exposed to amphetamine (AMPH, 4mg/kg SC), evaluating classic biological markers. AMPH administration itself augmented the plasma hypothalamic-pituitary-adrenal (HPA) hormones, adrenocorticotropin (ACTH) and corticosterone, without affecting plasma glucose levels. By contrast, this drug dampened the peripheral HPA axis, as well as the response of glucose to the three stressors. We also found that AMPH administration completely blocked the forced swim-induced expression of the corticotropin-releasing hormone (hnCRH) and it partially reduced c-fos expression in the paraventricular nucleus of the hypothalamus (PVN). Indeed, this negative synergy in the forced swim test could even be observed with a lower dose of AMPH (1mg/kg, SC), a dose that is usually received in self-administration experiments. In conclusion, when rats that receive AMPH are subjected to stress, a negative synergy occurs that dampens the prototypic peripheral physiological response to stress and activation of the PVN.
    Psychoneuroendocrinology 10/2015; 63:94-101. DOI:10.1016/j.psyneuen.2015.09.006 · 4.94 Impact Factor
    • "On the other hand, there are different social experiences that induce social stress in animals , such as maternal deprivation, social isolation, crowding or social defeat (Lu et al., 2003; Miczek et al., 2008; Ribeiro Do Couto et al., 2009; Shaham et al., 2003). All these stimuli trigger nervous and hormonal mechanisms of stress that lead to neurochemical and behavioral adaptations, making animals more prone to drug-seeking (Goeders, 2002; Logrip et al., 2012; Marinelli and Piazza, 2002; Miczek et al., 2008; Moffett et al., 2007). Social defeat stress is a naturalistic model of stress that involves an agonistic encounter between conspecifics and is thought to represent a stressor of ecological and ethological validity in mice (Tornatzky and Miczek, 1993). "
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    ABSTRACT: Stressful experiences modify activity in areas of the brain involved in the rewarding effects of psychostimulants. In the present study we evaluated the influence of acute social defeat (ASD) on the conditioned rewarding effects of cocaine in adolescent (PND 29-32) and adult (PND 50-53) male mice in the conditioned place preference (CPP) paradigm. Experimental mice were exposed to social defeat in an agonistic encounter before each session of conditioning with 1 mg/kg or 25 mg/kg of cocaine. The effects of social defeat on corticosterone levels were also evaluated. Adult mice exposed to ASD showed an increase in the conditioned reinforcing effects of cocaine. Only these mice developed cocaine-induced CPP with the subthreshold dose of cocaine, and they needed a higher number of extinction sessions for the 25 mg/kg cocaine-induced CPP to be extinguished. In adolescent mice, on the other hand, ASD reduced the conditioned reinforcing effects of cocaine, since CPP was not produced with the lower dose of cocaine and was extinguished faster when they were conditioned with 25 mg/kg. Adult mice exposed to social defeat displayed higher levels of corticosterone than their controls and adolescent mice. Our results confirm that the effect of social defeat stress on the acquisition and reinstatement of the CPP induced by cocaine varies depending on the age at which this stress is experienced. Copyright © 2015. Published by Elsevier Inc.
    Pharmacology Biochemistry and Behavior 05/2015; 135. DOI:10.1016/j.pbb.2015.05.008 · 2.78 Impact Factor
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    • "In a recent study, we observed that the activity of the hypothalamic–pituitary–adre nal axis, as reflected in an increased cortisol level, increased only in males in response to whole-body cooling [45]. There is evidence that glucocorticoids can partly influence central dopamine release within the brain [24] [35] [37] [41]. Thus, in contrast to the effects of heat [23], the increased central dopaminergic activity during cold exposure in males may increase their central motivation to perform exercise and may subsequently reduce fatigue during voluntary exercise [6] [17] [23] [29]. "
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    ABSTRACT: The effects of cold stress on exercise performance and fatigue have been thoroughly investigated only in males, and thus the general understanding of these effects relates only to males. The aim of this study was to determine whether whole-body cooling has different effects on performance during fatiguing exercise in males and females. Thirty-two subjects (18 males and 14 females) were exposed to acute cold stress by intermittent immersion in 14°C water until their rectal temperature reached 35.5°C or for a maximum of 170 min. Thermal responses and motor performance were monitored before and after whole-body cooling. Whole-body cooling decreased rectal, muscle and mean skin temperatures in all subjects (p<0.05), and these changes did not differ between males and females. Cold stress decreased the fatigue index (FI) of a sustained 2-min maximal voluntary contraction (MVC) only in males (p<0.05). There were no sex differences in central and peripheral fatigability, or muscle electromyographic activity. This observed sex difference (i.e., body cooling-induced decrease in the FI of a sustained MVC in males but not in females) supports the view of sex effects on performance during fatiguing exercise after whole-body cooling. Copyright © 2015 Elsevier Inc. All rights reserved.
    Cryobiology 05/2015; 71(1). DOI:10.1016/j.cryobiol.2015.04.012 · 1.59 Impact Factor
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