Thermal antinociceptive responses to alcohol in DBA/2J and C57BL/6J inbred male and female mouse strains

White, Alyssa; Caillaud, Martial; Carper, Moriah; Poklis, Justin L.; Miles, Michael F.; Damaj, M. Imad

doi:10.1016/j.bbr.2022.114087

Cited by 9 publications

(5 citation statements)

References 35 publications

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“…Our behavioral examination of basal and post-ethanol hot plate latency revealed a significant antinociceptive effect of ethanol, congruent with rodent [16,18] and human [5] analgesia literature. There was no difference in hot plate latency between ethanol and control groups by Day 5 nociception testing, though, due to an increase in latency in vehicle-receiving mice.…”

Section: Discussionsupporting

confidence: 86%

“…Hot plate testing protocols were adapted from White et al (2020), which showed 1) 2.0 g/kg oral gavage ethanol produces maximum antinociception at 30 minutes post-administration 2) this dose of ethanol shows no locomotor effects in B6 mice and a small locomotor effect in D2 mice 3) baseline hot plate testing (as in the current design) does not interfere with post-gavage thermal nociception (i.e. post-saline Day 1 hot plate latency should be indistinguishable from Baseline)[18]. After acclimation the testing room overnight, mice were tested for baseline 55°C hot plate latency (Thermojust Apparatus, Columbus, OH) (Figure S1).…”

Section: Methodsmentioning

confidence: 99%

“…Recently, studies in rodent model organisms have described specific roles for opioid receptors and GABAergic signaling pathways in alcohol analgesia [16][17][18]. However, these systems do not account for all the variation in alcohol-induced analgesia.…”

Section: Introductionmentioning

confidence: 99%

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Identification of ethanol analgesia quantitative trait loci and candidate genes in BXD recombinant inbred mouse lines

Rogers,

White,

Damaj

et al. 2024

Preprint

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Alcohol consumption produces acute analgesic effects, and people experiencing pain conditions may drink alcohol to alleviate discomfort. However, tolerance to the analgesic properties of alcohol could prompt escalating consumption and dependence. Both nociception and alcohol-induced analgesia are under significant genetic control. Understanding the genetic architecture of these processes could inform better treatment options for people with pain conditions. This study aims to identify quantitative trait loci (QTL) driving variation in ethanol-induced analgesia across BXD recombinant inbred mouse lines. Male and female mice from 62 BXD strains received ethanol or saline oral gavage for five days and were tested for hot plate (HP) latency at baseline, Day 1, and Day 5. QTL mapping of HP phenotypes identified a significant provisional QTL on chromosome 17 for Day 1 HP latency in mice receiving ethanol. An additional highly suggestive QTL was present on chromosome 9 for the difference in pre- and post-ethanol thermal nociception. Candidate genes within QTL support intervals were provisionally identified using HP phenotypic correlations to transcriptomic database, expression QTL analysis, and other bioinformatics inquiries. The combined behavioral and bioinformatic analyses yielded strong ethanol analgesia candidate genes, specificallyMyo6. Thus, the results of this genetic study of ethanol-induced analgesia in BXD mouse strains may contribute significantly to our understanding of the molecular basis for individual variation in the analgesic response to acute ethanol.

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Section: Discussionsupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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Identification of ethanol analgesia quantitative trait loci and candidate genes in BXD recombinant inbred mouse lines

Rogers,

White,

Damaj

et al. 2024

Preprint

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“…Sex differences in AWH in these procedures are likely dependent on the method of alcohol exposure (voluntary vs. forced; continuous vs. intermittent), dose of alcohol, duration of exposure, and/or time points during which testing is conducted during withdrawal. The previous literature shows that male mice are more susceptible to the antinociceptive effects of alcohol than females (Bilbao et al., 2019; White et al., 2023). Sex differences have also been observed in pain processing (Mogil, 2020), and our observation of increased mechanical sensitivity after DID in males may be related to these differences.…”

Section: Discussionmentioning

confidence: 96%

Histone deacetylase inhibitor decreases hyperalgesia in a mouse model of alcohol withdrawal‐induced hyperalgesia

Aguilar,

De Carvalho,

Chen

et al. 2024

Alcohol, Clinical and Experimental Research

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BackgroundAlcohol withdrawal‐induced hyperalgesia (AWH) is characterized as an increased pain sensitivity observed after cessation of chronic alcohol use. Alcohol withdrawal‐induced hyperalgesia can contribute to the negative affective state associated with abstinence and can increase susceptibility to relapse. We aimed to characterize pain sensitivity in mice during withdrawal from two different models of alcohol exposure: chronic drinking in the dark (DID) and the Lieber–DeCarli liquid diet. We also investigated whether treatment with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), could ameliorate AWH in mice treated with the Lieber–DeCarli diet.MethodsMale and female C57BL/6J mice were used for these studies. In the DID model, mice received bottles of 20% ethanol or water during the dark cycle for 4 h per day on four consecutive days per week for 6 weeks. Peripheral mechanical sensitivity was measured weekly the morning of Day 5 using von Frey filaments. In the Lieber–DeCarli model, mice received ethanol (5% v/v) or control liquid diet for 10 days, along with a single binge ethanol gavage (5 g/kg) or control gavage, respectively, on Day 10. Peripheral mechanical sensitivity was measured during the liquid diet administration and at 24 and 72 h into ethanol withdrawal. An independent group of mice that received the Lieber–DeCarli diet were administered SAHA (50 mg/kg, i.p.) during withdrawal.ResultsMale mice exhibited mechanical hypersensitivity after consuming ethanol for 5 weeks in the DID procedure. In the Lieber–DeCarli model, ethanol withdrawal led to hyperalgesia in both sexes. Suberoylanilide hydroxamic acid treatment during withdrawal from the ethanol liquid diet alleviated AWH.ConclusionsThese results demonstrate AWH in mice after chronic binge drinking in males and after Lieber–DeCarli liquid diet administration in both sexes. Like previous findings in rats, HDAC inhibition reduced AWH in mice, suggesting that epigenetic mechanisms are involved in AWH.

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“…Furthermore, we did not test enough doses to fit a dose–response curve for ED 50 calculation, such that the antinociceptive potency of EtOH cannot be compared between CTL and LBN females. The fact that the antinociceptive effect of EtOH did not reach significance in the CTL females, while it did under identical testing conditions and comparable baseline thresholds in C57BL/6J males (Okhuarobo, Kreifeldt, et al, 2020) suggests that C57BL/6J females may be less sensitive than males, which is consistent with a recent report (White et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

Influence of early‐life adversity on responses to acute and chronic ethanol in female mice

Okhuarobo

Angelo

Bolton

et al. 2022

Alcohol: Clinical and Experimental Research

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Background Stressful early‐life experiences increase the risk of developing an alcohol use disorder. We previously found that male C57BL/6J mice reared under limited bedding and nesting (LBN) conditions, a model of early‐life adversity, escalate their ethanol intake in limited‐access two‐bottle choice (2BC) sessions faster than control (CTL)‐reared counterparts when exposed to chronic intermittent ethanol (CIE) vapor inhalation. However, the alcohol consumption of female littermates was not affected by LBN or CIE. In the present study, we sought to determine whether this phenotype reflected a general insensitivity of female mice to the influence of early‐life stress on alcohol responses. Methods In a first experiment, CTL and LBN females with a history of 2BC combined or not with CIE were tested in affective and nociceptive assays during withdrawal. In a second group of CTL and LBN females, we examined ethanol‐induced antinociception, sedation, plasma clearance, and c‐Fos induction. Results In females withdrawn from chronic 2BC, CIE increased digging, reduced grooming, and increased immobility in the tail suspension test regardless of early‐life history. In contrast, LBN rearing lowered mechanical nociceptive thresholds regardless of CIE exposure. In females acutely treated with ethanol, LBN rearing facilitated antinociception and delayed the onset of sedation without influencing ethanol clearance rate or c‐Fos induction in the paraventricular nucleus of the hypothalamus, paraventricular nucleus of the thalamus, central nucleus of the amygdala, or auditory cortex. Conclusion CIE withdrawal produced multiple indices of negative affect in C57BL/6J females, suggesting that their motivation to consume alcohol may differ from air‐exposed counterparts despite equivalent intake. Contrasted with our previous findings in males, LBN‐induced mechanical hyperalgesia in chronic alcohol drinkers was specific to females. Lower nociceptive thresholds combined with increased sensitivity to the acute antinociceptive effect of ethanol may contribute to reinforcing ethanol consumption in LBN females but are not sufficient to increase their intake.

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Thermal antinociceptive responses to alcohol in DBA/2J and C57BL/6J inbred male and female mouse strains

Cited by 9 publications

References 35 publications

Identification of ethanol analgesia quantitative trait loci and candidate genes in BXD recombinant inbred mouse lines

Identification of ethanol analgesia quantitative trait loci and candidate genes in BXD recombinant inbred mouse lines

Histone deacetylase inhibitor decreases hyperalgesia in a mouse model of alcohol withdrawal‐induced hyperalgesia

Influence of early‐life adversity on responses to acute and chronic ethanol in female mice

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