The Endocrine System and Alcohol Drinking in Females

Finn, Deborah A.

doi:10.35946/arcr.v40.2.02

Cited by 35 publications

(29 citation statements)

References 106 publications

(254 reference statements)

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“…Additionally, treatment with the synthetic estrogen 17β‐estradiol‐3‐benzoate in ovariectomized mice restored drinking patterns to that of control (Satta et al, 2018), implicating estrogen levels play a pertinent role in driving intake in female mice. Furthermore, activation of both α‐ and β‐estrogen receptors within the hypothalamus can enhance dopaminergic signaling within the hypothalamus increasing output of the paraventricular nucleus and HPA axis responsivity in females (Finn, 2020; Rachdaoui & Sarkar, 2017). Thus through this mechanism, estrogen may promote higher drinking patterns in females due to increased levels of dopamine and glucocorticoids within the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Ethanol consumption activates a subset of arcuate nucleus pro‐opiomelanocortin (POMC)‐producing neurons: a c‐fos immunohistochemistry study

Hood

Nagy

Leyrer‐Jackson

2022

Physiological Reports

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Ethanol activates various opioid peptide‐containing circuits within the brain that may underlie its motivational and rewarding effects. One component of this circuitry consists of neurons located in the arcuate nucleus (ArcN) of the hypothalamus which express pro‐opiomelanocortin (POMC), an opioid precursor peptide that is cleaved to form bioactive fragments including β‐endorphin and α‐melanocyte stimulating hormone. In this study, we sought to determine if ethanol intake activates ArcN POMC neurons as measured by expression of the immediate early gene c‐fos. Male and female POMC‐EGFP mice underwent drinking‐in‐the‐dark (DID) procedures for 3 consecutive days (2 h/day) and were allowed to consume either ethanol (20% v/v), saccharin (0.2% w/v), or water. On the fourth day of DID procedures, animals were allowed to consume their respective solutions for 20 min, and 1 h following the session brains were harvested and processed for c‐fos immunohistochemistry and co‐localization with EGFP. Our results indicate that ethanol intake activates a subset (~15–20%) of ArcN POMC neurons, whereas saccharin or water intake activates significantly fewer (~5–12%) of these neurons. The percent of activated POMC neurons did not correlate with blood ethanol levels at the time of tissue collection, and activation appeared to be distributed throughout the rostrocaudal axis of the ArcN. No sex differences were observed in the degree of neuronal activation across drinking solutions. These findings indicate a preferential activation of ArcN POMC neurons by ethanol consumption, strengthening the notion that ethanol activates endogenous opioid systems in the brain which may underlie its motivational properties.

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Section: Discussionmentioning

confidence: 99%

Ethanol consumption activates a subset of arcuate nucleus pro‐opiomelanocortin (POMC)‐producing neurons: a c‐fos immunohistochemistry study

Hood

Nagy

Leyrer‐Jackson

2022

Physiological Reports

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“…Corticotropin releasing factor (CRF) in the paraventricular nucleus of the hypothalamus (PVN) controls the pituitary response to stress ( Turnbull and Rivier, 1997 ). High levels of glucocorticoids exert negative feedback to shut off the hypothalamic-pituitary-adrenal (HPA) axis, but they also exert positive feedback at the level of the amygdala ( Makino et al, 2002 ; Edwards et al, 2015 ; Finn, 2020 ). Acute administration of most drugs of abuse, including ethanol, activates the HPA axis, but these changes are blunted or dysregulated with repeated drug exposure ( Koob, 2008 ; Richardson et al, 2008 ).…”

Section: Introductionmentioning

confidence: 99%

Sensitivity and Resilience to Predator Stress-Enhanced Ethanol Drinking Is Associated With Sex-Dependent Differences in Stress-Regulating Systems

Alavi

Ryabinin

Helms

et al. 2022

Front. Behav. Neurosci.

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Stress can increase ethanol drinking, and evidence confirms an association between post-traumatic stress disorder (PTSD) and the development of alcohol use disorder (AUD). Exposure to predator odor is considered a traumatic stressor, and predator stress (PS) has been used extensively as an animal model of PTSD. Our prior work determined that repeated exposure to intermittent PS significantly increased anxiety-related behavior, corticosterone levels, and neuronal activation in the hippocampus and prefrontal cortex in naïve male and female C57BL/6J mice. Intermittent PS exposure also increased subsequent ethanol drinking in a subgroup of animals, with heterogeneity of responses as seen with comorbid PTSD and AUD. The present studies built upon this prior work and began to characterize “sensitivity” and “resilience” to PS-enhanced drinking. Ethanol drinking was measured during baseline, intermittent PS exposure, and post-stress; mice were euthanized after 24-h abstinence. Calculation of median and interquartile ranges identified “sensitive” (>20% increase in drinking over baseline) and “resilient” (no change or decrease in drinking from baseline) subgroups. Intermittent PS significantly increased subsequent ethanol intake in 24% of male (↑60%) and in 20% of female (↑71%) C57BL/6J mice in the “sensitive” subgroup. Plasma corticosterone levels were increased significantly after PS in both sexes, but levels were lower in the “sensitive” vs. “resilient” subgroups. In representative mice from “sensitive” and “resilient” subgroups, prefrontal cortex and hippocampus were analyzed by Western Blotting for levels of corticotropin releasing factor (CRF) receptor 1, CRF receptor 2, CRF binding protein, and glucocorticoid receptor, vs. separate naïve age-matched mice. In prefrontal cortex, CRF receptor 1, CRF receptor 2, CRF binding protein, and glucocorticoid receptor levels were significantly higher in “sensitive” vs. naïve and “resilient” mice only in females. In hippocampus, CRF receptor 1, CRF receptor 2 and glucocorticoid receptor levels were significantly lower in “resilient” vs. naïve and “sensitive” mice across both sexes. These results indicate that sex strongly influences the effects of ethanol drinking and stress on proteins regulating stress and anxiety responses. They further suggest that targeting the CRF system and glucocorticoid receptors in AUD needs to consider the comorbidity of PTSD with AUD and sex of treated individuals.

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“…One consideration is that the determinants of differential responsivity to reproductive hormones might span the susceptibility for differential responsivity to a broader range of chemicals, especially ones with shared pharmacological properties. Alcohol affects both the serum levels of neuroactive reproductive steroids (estradiol, progesterone, and its reduced metabolite allopregnanolone) and their mediation of neurotransmission via ligand‐gated ion channel receptors (N‐methyl‐D‐aspartate receptor, γ‐aminobutyric acid A receptor [GABA A R]) that play important roles in seizure occurrence 3,4 . Alcohol shares with allopregnanolone the propensity for preferential binding to α4δ subunits of the extrasynaptic GABA A R that is important in tonic neuroinhibition 5,6 .…”

Section: Introductionmentioning

confidence: 99%

“…Alcohol affects both the serum levels of neuroactive reproductive steroids (estradiol, progesterone, and its reduced metabolite allopregnanolone) and their mediation of neurotransmission via ligand-gated ion channel receptors (N-methyl-D-aspartate receptor, γaminobutyric acid A receptor [GABA A R]) that play important roles in seizure occurrence. 3,4 Alcohol shares with allopregnanolone the propensity for preferential binding to α4δ subunits of the extrasynaptic GABA A R that is important in tonic neuroinhibition. 5,6 Both alcohol and allopregnanolone exhibit tolerance and have crosstolerance to each other.…”

Section: Introductionmentioning

confidence: 99%

Association between family history of alcohol use disorder and catamenial epilepsy

Herzog

2022

Epilepsia

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The purpose of this investigation was to determine whether a family history of alcohol use disorder (AUD) might be a risk factor and possible clinical biomarker for catamenial epilepsy. The retrospective case-control data came from 119 women, aged 13-48 years, with intractable seizures. We report the relative risk for positive family history of AUD among women with catamenial epilepsy (Group 1) relative to women with noncatamenial epilepsy (Group 2). The risk ratio (RR) for positive AUD history for Group 1 (n = 59) relative to Group 2 (n = 60) was 3.46 (95% confidence interval = 1.36-8.76, p = .009). The RRs were significant for women who had the (C1) perimenstrual (p = .009) and (C3) entire luteal phase (p = .003) patterns but not the (C2) preovulatory pattern. AUD history had a high specificity of 91.7% (55/60) but relatively low sensitivity of 28.8% (17/59) for the prediction of catamenial epilepsy. The positive predictive value was 77.3% (17/22), whereas the negative predictive value was 56.7% (55/97). AUD history is a highly specific biomarker for catamenial epilepsy but has relatively low sensitivity for its detection.Further investigation may identify additional biomarkers that are more efficient than seizure-menses calendars.

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The Endocrine System and Alcohol Drinking in Females

Cited by 35 publications

References 106 publications

Ethanol consumption activates a subset of arcuate nucleus pro‐opiomelanocortin (POMC)‐producing neurons: a c‐fos immunohistochemistry study

Ethanol consumption activates a subset of arcuate nucleus pro‐opiomelanocortin (POMC)‐producing neurons: a c‐fos immunohistochemistry study

Sensitivity and Resilience to Predator Stress-Enhanced Ethanol Drinking Is Associated With Sex-Dependent Differences in Stress-Regulating Systems

Association between family history of alcohol use disorder and catamenial epilepsy

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