Voluntary elevated ethanol consumption in adolescent Sprague-Dawley rats: Procedural contributors and age-specificity

Hosová, Dominika; Spear, Linda P.

doi:10.1016/j.alcohol.2019.02.003

Cited by 7 publications

(3 citation statements)

References 65 publications

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“…Importantly, in comparison with intragastric infusions or subcutaneous injections (Braconi et al, 2010;Crews et al, 2000;Sircar & Sircar, 2005), the voluntary EtOH intake paradigm used in the present study is substantially less stressful (Evrard et al, 2006;Hosov a & Spear, 2019;Odeon et al, 2015), as it might mimic human drinking settings, yielding clinically relevant data. In addition, in the intermittent drinking regimen, grouphoused adolescent animals from both sexes did not exhibit an escalation in EtOH intake, as reported by Skelly et al (2015).…”

Section: Discussionmentioning

confidence: 99%

Behavioural alterations induced by intermittent ethanol intake and noise exposure in adolescent rats

Buján

D’Alessio

Serra

et al. 2022

Eur J of Neuroscience

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Alcohol intake and exposure to noise are common activities of human adolescents performed in entertainment contexts worldwide that can induce behavioural disturbances. Therefore, the aim of the present work was to investigate in an experimental model of adolescent animals whether noise exposure and intermittent ethanol intake, when present individually or sequentially, might be able to modify different behaviours. Adolescent Wistar rats of both sexes were subjected to voluntary intermittent ethanol intake for 1 week followed by exposure to noise for 2 h and tested in a battery of behavioural tasks. Data show that males exposed to noise experienced a deficit in associative memory (AM), increase in anxiety-like behaviours (ALB) and altered reaction to novelty (RN) when compared with sham animals, whereas females also showed an increase in risk assessment behaviours (RABs) and a decrease in exploratory activity (EA). In contrast, ethanol intake induced an increase in RAB and RN in males and females, whereas females also showed a deficit in AM and EA as well as an increase in ALB. When ethanol was ingested before noise exposure, most parameters were counteracted both in male and females, but differed among sexes. In consequence, it could be hypothesized that an environmental acute stressor like noise might trigger a behavioural counteracting induced by a previous repeated exposure to a chemical agent such as ethanol, leading to a compensation of a non-adaptive behaviour and reaching a better adjustment to the environment.

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Section: Discussionmentioning

confidence: 99%

Behavioural alterations induced by intermittent ethanol intake and noise exposure in adolescent rats

Buján

D’Alessio

Serra

et al. 2022

Eur J of Neuroscience

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“…However, we note that this said study in SD rats employed a 2 hr access to ethanol for 8 days as compared to the ~11 week IA2BC model employed in our study. In another study with SD rats, adolescent rats consumed significantly higher amounts of an ethanol-Boost1 solution as compared to adults, however no sex-based difference was seen in ethanol consumption in adult rats [58]. Thus, our finding that adult female SD rats show lower ethanol consumption and preference as compared to adult males could be attributed to several factors including strain, study paradigm, type of alcohol presented etc.…”

Section: Plos Onementioning

confidence: 47%

Desformylflustrabromine (dFBr), a positive allosteric modulator of α4β2 nicotinic acetylcholine receptors decreases voluntary ethanol consumption and preference in male and female Sprague-Dawley rats

et al. 2022

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Alcohol use disorder is a medical condition that impacts millions of individuals worldwide. Although there are a few pharmacotherapeutic options for alcohol-dependent individuals; there is a need for the development of novel and more effective therapeutic approaches. Alcohol and nicotine are commonly co-abused, and there is evidence that neuronal nicotinic acetylcholine receptors (nAChRs) play a role in both alcohol and nicotine dependence. Desformylflustrabromine (dFBr), a positive allosteric modulator of the α4β2 nAChRs has been shown to reduce nicotine intake, compulsive-like behavior and neuropathic pain in animal models. dFBr has also been previously shown to cross the blood-brain-barrier. We have recently shown that dFBr can attenuate the response to an acute, hypnotic dose of ethanol, via β2 nAchR. Here, we have investigated the effect of dFBr in modulating ethanol consumption using the intermittent access two-bottle choice (IA2BC) model of voluntary ethanol consumption in male and female Sprague Dawley rats. We show that dFBr selectively reduced ethanol but not sucrose consumption in the IA2BC model. Furthermore, dFBr decreased preference for ethanol in both male and female rats. No rebound increase in ethanol intake was observed after the washout period after dFBr treatment. The ability of dFBr to decrease ethanol consumption, along with its previously demonstrated ability to decrease nicotine self-administration in rodents, suggest that dFBr is an attractive therapeutic candidate to target both nicotine and alcohol abuse.

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“…Rats had access to EtOH for 5 days, and daily EtOH self‐administration was measured for those 5 days, before EtOH was removed. While we did not measure blood EtOH concentration, similar levels of EtOH self‐administration result in modest blood EtOH levels (Hosova & Spear, 2019; Simms et al, 2008, 2010). At least 5 days after EtOH removal, we began recording α3β4 nAChR currents in LDTg neurons using focal application of ACh (1 mM), this time from a single picospritzer pipette, in acute brain slices, taken from 10 rats.…”

Section: Resultsmentioning

confidence: 97%

Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum

Abburi

McDaid

2021

Alcoholism Clin & Exp Res

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Background Nicotinic acetylcholine receptors (nAChRs) play a key role in the rewarding effects of ethanol (EtOH), and while several nAChR subtypes have been implicated, attention has recently shifted to a role for the α3β4 nAChR. The laterodorsal tegmental nucleus (LDTg), a brainstem cholinergic nucleus that sends excitatory projections to the ventral tegmental area, is an Integral part of the brain reward pathway. Here we investigate a potential role for LDTg α3β4 nAChRs in EtOH self‐administration and reward. Methods Sprague‐Dawley rats were given ad libitum access to a 20% EtOH solution, as part of a two‐bottle choice paradigm. Approximately 1 week after removal of EtOH access, we measured LDTg α3β4 nAChR current responses to focal application of acetylcholine (ACh), using whole‐cell patch clamp electrophysiology recordings in acute brain slices. In addition, we used whole‐cell electrophysiology to assess the acute effects of EtOH on the sensitivity of LDTg α3β4 nAChRs. Results Focal application of ACh onto LDTg neurons resulted in large α3β4 nAChR‐mediated inward currents, the magnitude of which showed a positive correlation with levels of EtOH self‐administration. In addition, using brain slices taken from EtOH‐naïve rats, bath application of EtOH resulted in a moderate potentiation of LDTg α3β4 nAChR sensitivity. Conclusions Using a rat model, increased α3β4 nAChR function was associated with greater EtOH self‐administration, with α3β4 nAChR function also acutely potentiated by EtOH. Assuming that similar findings apply to humans, the α3β4 nAChR could be a therapeutic target in the treatment of EtOH use disorder.

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Voluntary elevated ethanol consumption in adolescent Sprague-Dawley rats: Procedural contributors and age-specificity

Cited by 7 publications

References 65 publications

Behavioural alterations induced by intermittent ethanol intake and noise exposure in adolescent rats

Behavioural alterations induced by intermittent ethanol intake and noise exposure in adolescent rats

Desformylflustrabromine (dFBr), a positive allosteric modulator of α4β2 nicotinic acetylcholine receptors decreases voluntary ethanol consumption and preference in male and female Sprague-Dawley rats

Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum

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