Article

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: 3.67). 09/2002; 16(3):387-94. DOI: 10.1046/j.1460-9568.2002.02089.x
Source: PubMed

ABSTRACT 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.

0 Followers
 · 
185 Views
  • Source
    • "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]. "
    [Show abstract] [Hide abstract]
    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; DOI:10.1016/j.cryobiol.2015.04.012 · 1.64 Impact Factor
  • Source
    • "There is evidence that HPA-axis traits specifically undermine decision making. HPA disturbances predict addictive behavior (Koob & Kreek, 2007; Marinelli & Piazza, 2002; Putman, Antypa, Crysovergi, & van der Does, 2010; Sinha, 2008), and the relation between longterm HPA activity and pathological gambling (Wohl, Matheson, Young, & Anisman, 2008) may reflect altered punishment sensitivity. In nonclinical populations, the threat of financial loss (i.e., imminent poverty) chronically elevates cortisol (Haushofer, de Laat, & Chemin, 2012). "
    Psychological Science 09/2014; DOI:10.1177/0956797614546555 · 4.43 Impact Factor
  • Source
    • "This reward system is well-suited for glucocorticoid regulation since glucocorticoid and mineralocorticoid receptors, on which CRT acts, are abundant within the amygdala (de Kloet et al., 2005; Oitzl et al., 2010). A rich animal literature illustrates this, showing that exogenous or stress-induced glucocorticoids can up-regulate reward seeking and increase sensitivity for the reinforcing effects of drugs through NAcc dopamine release (Piazza and Le Moal, 1997; Marinelli and Piazza, 2002; de Jong and de Kloet, 2004). Although direct evidence for the involvement of CRT in reward-related behaviors in humans is scarce, a study in which CRTwas administered shows increased risk-taking after CRT (Putman et al., 2010a), which could reflect increased reward drive. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Research in rodents and humans has shown divergent effects of the glucocorticoids corticosterone and cortisol (CRT) on reward processing. In rodents, administration of CRT increases reward drive by facilitating dopamine release in the ventral striatum. In humans, correspondingly, risky decision-making increases when CRT levels are elevated. Human stress studies contrariwise show that elevated CRT is accompanied by a decrease in reward-related brain activity. There are however no direct insights into how CRT acts on the reward system in the human brain. Accordingly, we used pharmacological functional magnetic resonance imaging (pharmaco-fMRI) to investigate the effects of CRT on the brain's reward system. In a randomized within-subject design we administered a high dose of CRT (40 mg) and placebo to twenty healthy male volunteers on separate days, and used a monetary incentive delay task to assess the effects of the hormone on the striatum and the amygdala in anticipation of potential reward. In contrast to animal studies, we show that this high dose of CRT strongly decreases activity of the striatum in both reward and non-reward conditions. Furthermore, we observed reductions in activity in the basolateral amygdala, a key regulator of the brain's reward system. Crucially, the overall down-regulation of the brain's reward circuit was verified on the subjective level as subjects reported significantly reduced reward preference after CRT. In sum, we provide here direct evidence in humans that CRT acts on brain regions involved in reward-related behavior, that is, the basolateral amygdala and the striatum. Our findings suggest that CRT in the quantity and time course presently globally down-regulates the reward system, and thereby decreases motivational processing in general.
    Psychoneuroendocrinology 09/2014; 47. DOI:10.1016/j.psyneuen.2014.04.022 · 5.59 Impact Factor
Show more

Preview

Download
1 Download
Available from