Corticosterone concentrations in mice during ethanol drinking and withdrawal

Tabakoff, Boris; Jaffe, Randal C.; Ritzmann, Ronald F.

doi:10.1111/j.2042-7158.1978.tb13259.x

Cited by 157 publications

(58 citation statements)

References 13 publications

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“…In fact, when we initially reported that N/OFQ increases circulating ACTH and CORT concentrations in unstressed and mildly stressed rats (Devine et al, 2001), we reconciled our hormonal findings with the published behavioral data (Jenck et al, 1997;Griebel et al, 1999) on the basis that a variety of drugs that are anxiolytic can also increase circulating CORT concentrations in unstressed or mildly stressed rats (Ellis, 1966;Kakihana et al, 1968;Marc and Morselli, 1969;Tabakoff et al, 1978;Rivier et al, 1984;Matheson et al, 1988Matheson et al, , 1997ade Boer et al, 1991). However, the current findings indicate that the behavioral and hormonal effects of N/OFQ resemble the effects of drugs like FG 7142 File, 1985, 1986), yohimbine (Smythe et al, 1983;Suemaru et al, 1989), amphetamine (Knych and Eisenberg, 1979;, and caffeine (Spindel et al, 1983;Fall of which are anxiogenic in neophobic tests of anxiety, and all of which elevate circulating ACTH and/or CORT concentrations after acute administration.…”

Section: Anxiogenic Action Of N/ofqmentioning

confidence: 76%

Nociceptin/Orphanin FQ Increases Anxiety-Related Behavior and Circulating Levels of Corticosterone During Neophobic Tests of Anxiety

Fernandez

Misilmeri

Felger

et al. 2003

Neuropsychopharmacol

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Intracranial administration of nociceptin/orphanin FQ (N/OFQ) increases circulating concentrations of adrenocorticotrophic hormone and corticosterone in unstressed rats, and elevates the responsiveness of these hormones during mild stress. Furthermore, N/OFQ and its cognate receptor are both abundant in a variety of limbic nuclei, and stress exposure decreases neuronal N/OFQ content in forebrain neurons. In light of these and other findings, we examined the potential involvement of N/OFQ in regulation of anxiety-related behaviors in rats. In the open field, elevated plus maze, and dark-light neophobic tests, intracerebroventricular N/OFQ (1.0 pmole-1.0 nmole) increased the expression of anxiety-related behaviors. Specifically, N/OFQ increased the latency to enter, decreased the number of entries into, and decreased the time spent in the exposed or brightly lit environments of all three tests. N/OFQ also enhanced thigmotactic responses in the open field test. The effects of diazepam and of the benzodiazepine inverse agonist FG 7142 were also assessed in independent groups of rats. In all three tests, the behavioral effects of N/OFQ resembled the anxiogenic actions of FG 7142, and contrasted with the anxiolytic actions of diazepam. N/OFQ administration also increased circulating concentrations of corticosterone during anxiety testing, in comparison with the concentrations in vehicle-treated controls. We conclude that N/OFQ administration is anxiogenic, and elevates responsiveness of the hypothalamic pituitary-adrenal axis during neophobic tests of anxiety. This supports the possibility that N/OFQ neurotransmission participates in processing of emotionally-salient and stressful stimuli, and suggests that normal functioning of the N/OFQ system may be important in physiological and psychological well-being.

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Section: Anxiogenic Action Of N/ofqmentioning

confidence: 76%

Nociceptin/Orphanin FQ Increases Anxiety-Related Behavior and Circulating Levels of Corticosterone During Neophobic Tests of Anxiety

Fernandez

Misilmeri

Felger

et al. 2003

Neuropsychopharmacol

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“…The hyperactive HPA axis has also been shown during ethanol withdrawal after long-term exposure in animals and humans (Tabakoff et al, 1978;Wand, 1993). Furthermore, it has been shown that adrenalectomy prevents the development of ethanol preference in rats (Fahlke and Eriksson, 2000).…”

mentioning

confidence: 99%

Modulation of Cellular Expression of Glucocorticoid Receptor and Glucocorticoid Response Element-DNA Binding in Rat Brain during Alcohol Drinking and Withdrawal

Roy

Mittal²,

Zhang³

et al. 2002

J Pharmacol Exp Ther

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To define the molecular mechanisms of abnormal hypothalamic pituitary adrenal (HPA) axis during ethanol dependence, we investigated the effect of chronic ethanol treatment (15 days) and its withdrawal (24 h) on the expression of glucocorticoid receptors (GRs) and glucocorticoid response element (GRE)-DNA binding in the rat brain. The effects of chronic mianserin [serotonin (5-HT) 2A/2C antagonist] treatment on these parameters in various brain structures of control diet-fed and ethanolfed rats were also investigated. It was found that ethanol treatment and withdrawal significantly decreased the GR protein levels in cortical (cingulate gyrus, frontal, parietal, and piriform cortex) and amygdaloid (central, medial, and basolateral) structures and paraventricular nucleus (PVN) of hypothalamus of rats. It was also observed that ethanol treatment produced significant reductions in GR protein levels in various hippocampal structures (CA1, CA2, CA3, and dentate gyrus), but these changes were normalized during ethanol withdrawal. Ethanol treatment also significantly decreased GRE-DNA binding in rat cortex and hippocampus, which remained decreased in the cortex but reverted to normal in hippocampus during ethanol withdrawal. Chronic mianserin (alone) treatment had no effect on cortical GRE-DNA binding and GR protein levels in cortical, amygdaloid, or PVN structures but significantly decreased the GR protein expression in various hippocampal structures and GRE-DNA binding in whole hippocampus. However, when administered concurrently with ethanol treatment, mianserin significantly antagonized the reductions in cortical GRE-DNA binding and in GR protein expression in cortical, PVN, and central, but not medial and basolateral, amygdaloid structures during ethanol withdrawal. On the other hand, mianserin treatment along with ethanol administration significantly decreased the hippocampal GRE-DNA binding and GR protein expression in various hippocampal structures during ethanol withdrawal. Furthermore, ethanol treatment and its withdrawal or mianserin treatment had no effect on the neuron-specific nuclear protein levels in the various brain structures. Taken together, these results indicate that interaction of 5-HT 2A/2C receptors with GRs in cortical, central amygdaloid, and PVN structures may play a role in neural mechanisms of alcohol dependence. It is possible that decreased GR expression in PVN may be responsible for the abnormal HPA axis during ethanol exposure and withdrawal.

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“…Adrenocorticotropin was measured in 100 l of plasma by using an adrenocorticotropin enzyme-linked immunosorbent assay kit (ALPCO Diagnostics, Windham, NH). Blood ethanol levels were determined (in 20-l samples from the same mice used for the endocrine assays) by head-space gas chromatography, using a Varian, Inc. (Palo Alto, CA) 3800 gas chromatograph as described previously (Tabakoff et al, 1978).…”

Section: Methodsmentioning

confidence: 99%

“…A well established, but sometimes overlooked, fact about the physiologic actions of ethanol is that even modest doses of ethanol in humans or other animals can increase circulating levels of adrenocorticotropin and cortisol or corticosterone (Tabakoff et al, 1978;Rivier et al, 1984;Thiagarajan et al, 1988;Ogilvie et al, 1997).…”

mentioning

confidence: 99%

Type 7 Adenylyl Cyclase-Mediated Hypothalamic-Pituitary-Adrenal Axis Responsiveness: Influence of Ethanol and Sex

Pronko

Saba²,

Hoffman³

et al. 2010

J Pharmacol Exp Ther

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Although ethanol has been considered to be an anxiolytic agent, consumption of ethanol has also been shown to increase plasma adrenocorticotropin and glucocorticoids. The corticotrophin-releasing factor (CRF) receptor 1␣ (CRF-R1) is a G protein-coupled receptor that activates adenylyl cyclase (AC), leading to adrenocorticotropin (and subsequently glucocorticoid) release into the circulation. There are nine members of the membrane-bound AC family, and the type 7 AC (AC7) is most sensitive to ethanol, which enhances the responsiveness of AC7 to G protein-coupled receptor activation. We determined the time course of ethanol's effect on plasma adrenocorticotropin and corticosterone levels in male and female AC7 transgenic (Adcy7 huTG ) mice (in which AC7 is overexpressed in neural tissue) and AC7 heterozygous knockdown [Adcy7(ϩ/Ϫ)] mice (in which AC7 is underexpressed in neural tissue), and their respective littermate controls [wild type (WT)]. CRF-R1 mRNA and mRNA and protein for different forms of ACs were measured by using gene expression arrays, quantitative reverse transcription-polymerase chain reaction, and immunoblotting in pituitaries of all animals. Our results demonstrated increased levels of AC7 in pituitary of Adcy7 huTG mice and decreased levels in pituitary of Adcy7(ϩ/Ϫ) mice compared with WT animals. Male and female Adcy7 huTG mice displayed higher plasma adrenocorticotropin and corticosterone levels than WT and/or Adcy7(ϩ/Ϫ) mice after ethanol injection. Female mice displayed higher adrenocorticotropin and corticosterone levels after ethanol injection than males, regardless of genotype. The data provide evidence for an integral role of AC7 in the increase of plasma adrenocorticotropin and corticosterone levels during alcohol intoxication.

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Corticosterone concentrations in mice during ethanol drinking and withdrawal

Cited by 157 publications

References 13 publications

Nociceptin/Orphanin FQ Increases Anxiety-Related Behavior and Circulating Levels of Corticosterone During Neophobic Tests of Anxiety

Nociceptin/Orphanin FQ Increases Anxiety-Related Behavior and Circulating Levels of Corticosterone During Neophobic Tests of Anxiety

Modulation of Cellular Expression of Glucocorticoid Receptor and Glucocorticoid Response Element-DNA Binding in Rat Brain during Alcohol Drinking and Withdrawal

Type 7 Adenylyl Cyclase-Mediated Hypothalamic-Pituitary-Adrenal Axis Responsiveness: Influence of Ethanol and Sex

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