The hypothalamopituitary–adrenal axis and alcohol preference

O'Callaghan, Matthew J.; Croft, Adam P.; Jacquot, Catherine; Little, H.J.

doi:10.1016/j.brainresbull.2005.08.006

Cited by 34 publications

(32 citation statements)

References 32 publications

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“…Therefore, the decreases in consumption may have been due to artificially elevated GR function in this chronic stress state. In agreement with this analysis, it has been shown that while mifepristone has no effect on baseline drinking in mice, it blocks stress-induced increases in drinking caused by daily vehicle injections (O'Callaghan et al, 2005). In conditions where stress is limited, mifepristone has no effect on ethanol intake (Fahlke et al, 1994(Fahlke et al, , 1995(Fahlke et al, , 1996Lowery et al, 2010;Yang et al, 2008).…”

Section: Discussionsupporting

confidence: 63%

“…The literature is somewhat mixed when examining the effects of mifepristone on ethanol consumption as some authors have reported decreases in consumption following drug treatment (Koenig and Olive, 2004;O'Callaghan et al, 2005), while others have reported no change (Fahlke et al, 1994(Fahlke et al, , 1995(Fahlke et al, , 1996Lowery et al, 2010;Yang et al, 2008). Koenig and Olive (2004) demonstrated significant decreases in consumption using a limited-access, two-bottle-choice paradigm; however, it is important to note that the animals were fluid restricted for 23 h a day (O'Callaghan et al, 2005). Water restriction has been shown to activate the HPA axis and elevate CORT in rats (Aguilera et al, 1993;Kiss et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…The anti-GC activity of mifepristone has made it a potential treatment for Cushing's syndrome (Johanssen and Allolio, 2007) and neurological and psychological disorders (DeBattista and Belanoff, 2006;Gallagher and Young, 2006;Gallagher et al, 2005Gallagher et al, , 2008Wulsin et al, 2010;Young, 2006). The drug has also been examined in the self-administration of amphetamine (De Vries et al, 1996), cocaine (Deroche-Gamonet et al, 2003;Fiancette et al, 2010), morphine (Mesripour et al, 2008), and ethanol, where it has been shown to have either no effect or decrease baseline ethanol consumption (Fahlke et al, 1995;Jacquot et al, 2008;Koenig and Olive, 2004;Lowery et al, 2010;O'Callaghan et al, 2005;Roberts et al, 1995;Yang et al, 2008). However, the role of mifepristone in stress-induced reinstatement of ethanol-seeking is not known.…”

Section: Introductionmentioning

confidence: 99%

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Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Simms

Haass‐Koffler

Bito-Onon

et al. 2011

Neuropsychopharmacol

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Chronic ethanol exposure leads to dysregulation of the hypothalamic-pituitary-adrenal axis, leading to changes in glucocorticoid release and function that have been proposed to maintain pathological alcohol consumption and increase vulnerability to relapse during abstinence. The objective of this study was to determine whether mifepristone, a glucocorticoid receptor antagonist, plays a role in ethanol self-administration and reinstatement. Male, Long-Evans rats were trained to self-administer either ethanol or sucrose in daily 30 min operant self-administration sessions using a fixed ratio 3 schedule of reinforcement. Following establishment of stable baseline responding, we examined the effects of mifepristone on maintained responding and yohimbine-induced increases in responding for ethanol and sucrose. Lever responding was extinguished in separate groups of rats and animals were tested for yohimbine-induced reinstatement and corticosterone release. We also investigated the effects of local mifepristone infusions into the central amygdala (CeA) on yohimbine-induced reinstatement of ethanol-and sucrose-seeking. In addition, we infused mifepristone into the basolateral amygdala (BLA) in ethanol-seeking animals as an anatomical control. We show that both systemic and intra-CeA (but not BLA) mifepristone administration suppressed yohimbine-induced reinstatement of ethanol-seeking, while only systemic injections attenuated sucroseseeking. In contrast, baseline consumption, yohimbine-induced increases in responding, and circulating CORT levels were unaffected. The data indicate that the CeA plays an important role in the effects of mifepristone on yohimbine-induced reinstatement of ethanolseeking. Mifepristone may be a valuable pharmacotherapeutic strategy for preventing relapse to alcohol use disorders and, as it is FDA approved, may be a candidate for clinical trials in the near future.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Simms

Haass‐Koffler

Bito-Onon

et al. 2011

Neuropsychopharmacol

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“…The genotype dependent vulnerability to stress regarding psychostimulants and ethanol could result from strain differences in stress sensitivity of distinct neurobiological susbtrates. Thus, although they share common substrates (Phillips et al 1997;Sarnyai et al 2001;Marinelli and Piazza 2002;O'Callaghan et al 2005;de Vries and Schoffelmeer 2005;Pierce and Kumaresan 2006), ethanol and psychostimulants could exert reinforcing effects through distinct mechanisms (Pierce and Kumaresan 2006). Consequently, DBA mice could present a vulnerability to stress of the neurobiological systems involved in psychostimulants reinforcing effects, whereas C57 would present a vulnerability to stress of the neurobiological systems involved in ethanol reinforcing effects.…”

Section: Discussionmentioning

confidence: 88%

Gene–environment interactions in vulnerability to cocaine intravenous self-administration: a brief social experience affects intake in DBA/2J but not in C57BL/6J mice

2007

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“…suprachiasmatic nucleus; glutamate; serotonin; microdialysis; alcohol ETHANOL (EtOH) is highly disruptive to mammalian circadian physiological and behavioral rhythms, including those for melatonin (43, 75), glucocorticoids (2, 70), thyroid-stimulating hormone (20), body temperature (5, 21, 22, 94), and sleep (11, 27, 42, 43, 72). Also, disrupted circadian timing of hypothalamic-pituitary-adrenal axis function is associated with increased EtOH preference in experimental animals, and in humans, may be a risk factor for developing alcoholism and relapsing after abstinence (16,61,98). In a related manner, circadian-based sleep problems are implicated in the development of alcoholism and in abstinent alcoholics' propensity to relapse (73, 74).…”

mentioning

confidence: 98%

Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

Ruby

Prosser²,

DePaul³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Disrupted circadian rhythmicity is associated with ethanol (EtOH) abuse, yet little is known about how EtOH affects the mammalian circadian clock of the suprachiasmatic nucleus (SCN). Clock timing is regulated by photic and nonphotic inputs to the SCN involving glutamate release from the retinohypothalamic tract and serotonin (5-HT) from the midbrain raphe, respectively. Our recent in vitro studies in the SCN slice revealed that EtOH blocks photic phase-resetting action of glutamate and enhances the nonphotic phase-resetting action of the 5-HT1A,7 agonist, 8-OH-DPAT. To explore the basis of these effects in the whole animal, we used microdialysis to characterize the pharmacokinetics of intraperitoneal injection of EtOH in the hamster SCN extracellular fluid compartment and then studied the effects of such EtOH treatment on photic and serotonergic phase resetting of the circadian locomotor activity rhythm. Peak EtOH levels (approximately 50 mM) from a 2 g/kg injection occurred within 20-40 min with a half-life of approximately 3 h. EtOH treatment dose-dependently attenuated photic phase advances but had no effect on phase delays and, contrary to in vitro findings, markedly attenuated 8-OH-DPAT-induced phase advances. In a complementary experiment using reverse microdialysis to deliver a timed SCN perfusion of EtOH during a phase-advancing light pulse, the phase advances were blocked, similar to systemic EtOH treatment. These results are evidence that acute EtOH significantly affects photic and nonphotic phase-resetting responses critical to circadian clock regulation. Notably, EtOH inhibition of photic signaling is manifest through direct action in the SCN. Such actions could underlie the disruption of circadian rhythmicity associated with alcohol abuse.

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The hypothalamopituitary–adrenal axis and alcohol preference

Cited by 34 publications

References 32 publications

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Mifepristone in the Central Nucleus of the Amygdala Reduces Yohimbine Stress-Induced Reinstatement of Ethanol-Seeking

Gene–environment interactions in vulnerability to cocaine intravenous self-administration: a brief social experience affects intake in DBA/2J but not in C57BL/6J mice

Acute ethanol impairs photic and nonphotic circadian phase resetting in the Syrian hamster

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