Naloxone‐induced ACTH release: mechanism of action in humans

Jackson, Richard V.; Grice, Jeffrey E.; Hockings, G. I.; Torpy, David J.

doi:10.1111/j.1365-2265.1995.tb02612.x

Cited by 20 publications

(17 citation statements)

References 22 publications

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“…The administration of an opioid antagonist like naloxone releases the inhibitory opiate input to the hypothalamus and stimulates CRF release from the hypothalamus, ACTH release from the pituitary, and consequently, increases adrenal cortisol production. The increase in DOC levels observed in plasma monkey samples following a naloxone challenge is likely due to the increased hormonal secretion from the adrenal gland, and it is consistent with previous data showing that this opioid antagonist increases the release of ACTH and cortisol in both humans and nonhuman primates (Jackson et al 1995;Williams et al 2003).…”

Section: Discussionsupporting

confidence: 89%

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

et al. 2005

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Section: Discussionsupporting

confidence: 89%

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

et al. 2005

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“…Thus, administration of naloxone at the doses of 125 and 375 μg/kg, increased plasma deoxycorticosterone levels up to 86 and 97%, respectively. This is consistent with data showing an activation of the HPA axis and increased cortisol and ACTH levels in humans and non-human primates (Jackson et al, 1995; Wand et al, 1998; Williams et al, 2003). CRF (1 μg/kg) increased plasma deoxycorticosterone levels up to 111% while dexamethasone (130 μg/kg) decreased deoxycorticosterone levels by 42%, in agreement with a suppression of HPA axis activity.…”

Section: Identification Of a Potential Neuroactive Steroid Biomarker supporting

confidence: 93%

The role of neuroactive steroids in ethanol/stress interactions: proceedings of symposium VII at the Volterra conference on alcohol and stress, May 2008

Morrow

Biggio

Serra

et al. 2009

Alcohol

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This report summarizes the proceedings of the symposium VII on the role of neuroactive steroids in stress/alcohol interactions. The production of GABAergic neuroactive steroids, including (3α,5α)-3-hydroxypregnan-20-one (3α,5α-THP) and (3α,5α)-3,21-dihydroxypregnan-20-one (3α,5α-THDOC) is a consequence of both acute stress and acute ethanol exposure. Acute, but not chronic ethanol administration elevates brain levels of these steroids and enhances GABA A receptor activity. Neuroactive steroids modulate acute anticonvulsant effects, sedation, spatial memory impairment, anxiolytic-like, antidepressant-like and reinforcing properties of ethanol in rodents. Furthermore, these steroids participate in the homeostatic regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Therefore, it is not surprising that neuroactive steroids are involved in ethanol/stress interactions. Nevertheless, the interactions are complex and not well understood. This symposium addressed the role of neuroactive steroids in both stress and alcohol responses and their interactions. Professor Giovanni Biggio of the University of Cagliari, Italy presented the effects of juvenile isolation stress on neuroactive steroids, GABA A receptor expression and ethanol sensitivity. Professor Howard Becker of the Medical University of South Carolina, USA presented evidence for neuroactive steroid involvement in ethanol dependence and drinking behavior. Professor Patrizia Porcu of the University of North Carolina, USA described a potential neuroactive steroid biomarker that may predict heavy drinking in monkeys and mice. These presentations provide a framework for new theories on the nature of ethanol/stress interactions that may be amenable to therapeutic interventions.

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“…This observation is consistent with recent data supporting a direct action of naloxone on CRH neurons in the PVN of the hypothalamus, with subsequent activation of the pituitaryadrenal axis (32,33). This observation is consistent with recent data supporting a direct action of naloxone on CRH neurons in the PVN of the hypothalamus, with subsequent activation of the pituitaryadrenal axis (32,33).…”

supporting

confidence: 92%

“…As numerous studies have demonstrated that naloxone hydrochloride readily crosses the blood-brain barrier to exert a variety of central effects (32)(33)(34)(35), it is unlikely that the observed lack of CSF CRH or NE response after naloxone administration is due to poor penetration into the brain. Although the change in the CSF CRH concentration with time after yohimbine administration was significant (by one-way ANOVA), more rigorous comparisons across all three groups (yohimbine, naloxone, and placebo) did not reveal a significant drug effect.…”

mentioning

confidence: 99%

Cerebrospinal Fluid Corticotropin-Releasing Hormone in Healthy Humans: Effects of Yohimbine and Naloxone¹

Vythilingam¹,

Anderson²,

Owens

et al. 2000

The Journal of Clinical Endocrinology & Metabolism

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CRH neurons projecting from the paraventricular nucleus (PVN) of the hypothalamus to the median eminence control hypothalamic-pituitary-adrenal (HPA) axis activity. However, CRH neurons outside the PVN as well as PVN neurons projecting to sites other than the median eminence also contribute to the stress response and may play a role in mood and anxiety disorders. We have attempted to investigate possible noradrenergic and opioid regulation of these non-HPA CRH neurons. We hypothesized that yohimbine (an alpha2-adrenergic antagonist) would have stimulatory action on non-HPA CRH neurons, whereas naloxone (a mu-opioid receptor antagonist) would not have this effect. Adult normal volunteers received i.v. yohimbine (n = 5; 0.4 microg/kg), naloxone (n = 4; 125 microg/kg), or placebo (n = 3; 0.9% saline). Cerebrospinal fluid (CSF) was collected continuously, and concentrations of CSF CRH, CSF norepinephrine (NE), and plasma cortisol were measured. Administration of either yohimbine or naloxone caused significant increases in plasma cortisol concentrations over time. Although yohimbine robustly increased CSF NE levels and appeared to increase CSF CRH levels, these effects were not seen after naloxone or placebo administration. Intraindividual correlations were not observed between the measured concentrations of plasma cortisol and CSF CRH for any of the subjects. The results support the idea that CSF CRH concentrations reflect the activity of non-HPA CRH neurons. Although both yohimbine and naloxone stimulated the HPA axis, only yohimbine appeared to have stimulatory effects on central NE and non-HPA CRH.

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Naloxone‐induced ACTH release: mechanism of action in humans

Cited by 20 publications

References 22 publications

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

The role of neuroactive steroids in ethanol/stress interactions: proceedings of symposium VII at the Volterra conference on alcohol and stress, May 2008

Cerebrospinal Fluid Corticotropin-Releasing Hormone in Healthy Humans: Effects of Yohimbine and Naloxone¹

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Naloxone‐induced ACTH release: mechanism of action in humans

Cited by 20 publications

References 22 publications

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

Hypothalamic–pituitary–adrenal axis and ethanol modulation of deoxycorticosterone levels in cynomolgus monkeys

The role of neuroactive steroids in ethanol/stress interactions: proceedings of symposium VII at the Volterra conference on alcohol and stress, May 2008

Cerebrospinal Fluid Corticotropin-Releasing Hormone in Healthy Humans: Effects of Yohimbine and Naloxone1

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Cerebrospinal Fluid Corticotropin-Releasing Hormone in Healthy Humans: Effects of Yohimbine and Naloxone¹