Stress hormone responses to corticotropin-releasing hormone in substance abusers without severe comorbid psychiatric disease

Contoreggi, Carlo; Herning, Ronald I.; Na, Paul; Gold, Philip W.; Chrousos, George P.; Negro, P; Better, Warren; Cadet, Jean Lud

doi:10.1016/s0006-3223(03)00167-7

Cited by 45 publications

(25 citation statements)

References 26 publications

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“…Previous studies have shown that HPA axis hyperactivity may be associated with drug-taking behavior (12), and incomplete normalization of the HPA axis may be more relevant for predicting relapse than intense cravings (13). The follow-up investigation of the current study showed that HPA axis measures return to normal on the 30th day of abstinence.…”

Section: Discussionsupporting

confidence: 50%

Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis in Opioid Dependent Subjects: Effects of Acute and Protracted Abstinence

Zhang

Ren

Sheng

et al. 2008

The American Journal of Drug and Alcohol Abuse

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Section: Discussionsupporting

confidence: 50%

Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis in Opioid Dependent Subjects: Effects of Acute and Protracted Abstinence

Zhang

Ren

Sheng

et al. 2008

The American Journal of Drug and Alcohol Abuse

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“…Inbred lines of high anxiety-like behavior (HAB) rats show similar profiles to anxious clinical populations, with increased adrenocortical response (Landgraf et al, 1999) and greater activation in brain areas implicated in anxiety (Hasler et al, 2004; Salomé et al, 2004). Individuals abusing psychostimulant drugs such as cocaine also show compromised adrenocortical responses, indicating that dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis implicated in anxiety disorders, may contribute to aspects of addiction as well (Contoreggi et al, 2003). Rats phenotyped as high responders (e.g., rats that self-administer amphetamine and sucrose more readily) show a more robust corticosterone (CORT) response to novelty exposure (Cain, Saucier and Bardo, 2005; Piazza et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Housing environment modulates physiological and behavioral responses to anxiogenic stimuli in trait anxiety male rats

et al. 2014

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Environmental enrichment can modulate mild and chronic stress, responses to anxiogenic stimuli as well as drug vulnerability in a number of animal models. The current study was designed to examine the impact of postnatal environmental enrichment on selectively bred 4th generation high (HAn) and low anxiety (LAn) male rats. After weaning, animals were placed in isolated, social and enriched environments (e.g., toys, wheels, ropes, changed weekly). We measured anxiety-like behavior (ALB) on the elevated plus maze (EPM; trial 1 at PND 46, trial 2 at PND 63), amphetamine (0.5 mg/kg, IP)-induced locomotor behavior, basal and post anxiogenic stimuli changes in (1) plasma corticosterone, (2) blood pressure and (3) core body temperature. Initially, animals showed consistent trait differences on EPM with HAn showing more ALB but after 40 days in select housing, HAn rats reared in an enriched environment (EE) showed less ALB and diminished AMPH-induced activity compared to HAn animals housed in isolated (IE) and social environments (SE). In the physiological tests, animals housed in EE showed elevated adrenocortical responses to forced novel object exposure but decreased body temperature and blood pressure changes after an air puff stressor. All animals reared in EE and SE had elevated BDNF-positive cells in the central amygdala (CeA), CA1 and CA2 hippocampal regions and the caudate putamen, but these differences were most pronounced in HAn rats for CeA, CA1 and CA2. Overall, these findings suggest that environmental enrichment offers benefits for trait anxiety rats including a reduction in behavioral and physiological responses to anxiogenic stimuli and amphetamine sensitivity, and these responses correlate with changes in BDNF expression in the central amygdala, hippocampus and the caudate putamen.

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“…Nicotine's reinforcing effects are mediated in part by activation of the mesolimbic dopamine system to stimulate dopamine release (Corrigall et al, 1992;Di Chiara, 2000;Watkins et al, 2000). Activation of the hypothalamic-pituitary-adrenal (HPA) axis is also thought to contribute to drug abuse at several phases of the addictive process (Contoreggi et al, 2003;Heinrichs and Koob, 2004;Koob and Le Moal, 2001;Marinelli and Piazza, 2002;Sinha, 2001). Adrenocorticotropin hormone (ACTH) stimulation by corticotropin releasing factor (CRF) is one component of the integrated physiological response to 'stress' (Nemeroff, 1996;Tsigos and Chrousos, 2002).…”

Section: Introductionmentioning

confidence: 99%

Effects of Smoking Successive Low- and High-Nicotine Cigarettes on Hypothalamic–Pituitary–Adrenal Axis Hormones and Mood in Men

Mendelson

Goletiani

Sholar

et al. 2007

Neuropsychopharmacol

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Smoking one cigarette produces rapid nicotine dose-related increases in hypothalamic-pituitary-adrenal (HPA) axis hormones, mood, and heart rate, but relatively little is known about the effects of smoking several cigarettes successively. Twenty-four healthy adult men who met Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria for nicotine dependence provided informed consent. After overnight abstinence from smoking, men smoked three low-or high-nicotine cigarettes for 4 min each at 60 min intervals. Samples for nicotine and hormone analysis, Visual Analog Scale (VAS) ratings of subjective effects and heart rate were collected at 4, 8, 12, 16, 20, 30, 40, and 50 min after each cigarette. After low-nicotine cigarettes, nicotine levels, adrenocorticotropin hormone, and heart rate did not increase significantly, cortisol and dehydroepiandrosterone decreased significantly, and positive VAS ratings were lower but parallel to ratings after high-nicotine cigarette smoking. After high-nicotine cigarettes, peak nicotine levels increased monotonically. HPA axis hormones increased after smoking, but peak levels did not differ significantly after successive high-nicotine cigarettes. Positive VAS ratings and heart rate increased after each high-nicotine cigarette, but peak levels were lower after smoking the second and third cigarette. 'Craving' decreased significantly after smoking both low-and high-nicotine cigarettes, then gradually increased during the 60 min interval between cigarettes. These data are consistent with clinical reports that the first cigarette after overnight nicotine abstinence is most salient. Tolerance to the subjective and cardiovascular effects of nicotine developed rapidly during repeated cigarette smoking, but nicotine-stimulated increases in HPA axis hormones did not change significantly.

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Stress hormone responses to corticotropin-releasing hormone in substance abusers without severe comorbid psychiatric disease

Cited by 45 publications

References 26 publications

Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis in Opioid Dependent Subjects: Effects of Acute and Protracted Abstinence

Dysfunction of the Hypothalamic–Pituitary–Adrenal Axis in Opioid Dependent Subjects: Effects of Acute and Protracted Abstinence

Housing environment modulates physiological and behavioral responses to anxiogenic stimuli in trait anxiety male rats

Effects of Smoking Successive Low- and High-Nicotine Cigarettes on Hypothalamic–Pituitary–Adrenal Axis Hormones and Mood in Men

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