Ethanol‐Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression

Vilpoux, Catherine; Warnault, Vincent; Pierrefiche, Olivier; Daoust, M.; Naassila, Mickaël

doi:10.1111/j.1530-0277.2009.00916.x

Cited by 115 publications

(99 citation statements)

References 143 publications

(329 reference statements)

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“…The second relevant observation in the study is that acute administration of ethanol elicited an increase of cfos IR in the Arc, the PVN and CeA, but not in the LH, which is consistent with previous molecular evidence (Chang et al;Thiele et al, 1997;Vilpoux et al). Acute i.p.…”

Section: Discussionsupporting

confidence: 76%

“…ethanol administration (Chang et al). Also, short-time abstinence (hours or days) induced in rats an increase in c-fos immunoreactivity in all major part of the brain (for a review see, Vilpoux et al, 2009). In brief, molecular data in animal ethanol research indicates that ethanol exposure, both acute and chronic, significantly alters brain regional cellular activity as measured by c-fos immunoreactivity.…”

Section: Introductionmentioning

confidence: 99%

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Repeated Binge-Like Ethanol Administration During Adolescence cause Decreased C-Fos Immunoreactivity in Amygdala and Arcuate Nucleus in Adult Sprague-Dawley Rats

et al. 2014

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SUMMARY:Binge alcohol drinking during adolescence has been associated with neurotoxicity and increased risk for the development of alcohol use disorders. There is evidence that acute and chronic ethanol administration alters c-fos expression, an indirect index of cellular activity, in different brain regions in adult rats. We evaluate here if a binge-like pattern of ethanol exposure during adolescence has a relevant impact on basal and/or ethanol-stimulated regional c-fos activity during adulthood. For that aim, SpragueDawley rats PND 25 were saline pre-treated, (SP group) or binge-ethanol pre-treated (BEP group) for two-consecutive days, at 48-h intervals, over a 14-day period (PND 25 to PND 38). At adult stage (PND 63) and following 25 ethanol-free days, we evaluated c-fos immunoreactivity in response to saline or acute ethanol (1.5 or 3.0 g/kg) in the hypothalamus and amygdala. We found that acute ethanol administration dose-dependently increased c-fos activity in the the Paraventricular nucleus of the hypothalamus (PVN). Interestingly, binge-ethanol exposure during adolescence significantly reduced basal c-fos activity during adulthood in the Central nucleus of the amygdala (CeA) and the Arcuate nucleus of hypothalamus (Arc). We conclude that binge-like ethanol administration during adolescence causes long-term disturbances in basal neural activity in brain areas critically involved with ethanol consumption.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Repeated Binge-Like Ethanol Administration During Adolescence cause Decreased C-Fos Immunoreactivity in Amygdala and Arcuate Nucleus in Adult Sprague-Dawley Rats

et al. 2014

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“…Previous studies show that acute EtOH and acute stress individually activate microglia (Ahlers et al., 2015; Sugama et al., 2009) and neurons (Vilpoux et al., 2009; Watanabe et al., 1994) across multiple brain regions. However, whether the 2 interact to affect microglial or neuronal activation is unknown.…”

Section: Resultsmentioning

confidence: 99%

Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Walter

Vetreno

Crews

2017

Alcoholism Clin & Exp Res

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BackgroundCycles of alcohol and stress are hypothesized to contribute to alcohol use disorders. How this occurs is poorly understood, although both alcohol and stress activate the neuroimmune system—the immune molecules and cells that interact with the nervous system. The effects of alcohol and stress on the neuroimmune system are mediated in part by peripheral signaling molecules. Alcohol and stress both enhance immunomodulatory molecules such as corticosterone and endotoxin to impact neuroimmune cells, such as microglia, and may subsequently impact neurons. In this study, we therefore examined the effects of acute and chronic ethanol (EtOH) on the corticosterone, endotoxin, and microglial and neuronal response to acute stress.MethodsMale Wistar rats were treated intragastrically with acute EtOH and acutely stressed with restraint/water immersion. Another group of rats was treated intragastrically with chronic intermittent EtOH and acutely stressed following prolonged abstinence. Plasma corticosterone and endotoxin were measured, and immunohistochemical stains for the microglial marker CD11b and neuronal activation marker c‐Fos were performed.ResultsAcute EtOH and acute stress interacted to increase plasma endotoxin and microglial CD11b, but not plasma corticosterone or neuronal c‐Fos. Chronic EtOH caused a lasting sensitization of stress‐induced plasma endotoxin, but not plasma corticosterone. Chronic EtOH also caused a lasting sensitization of stress‐induced microglial CD11b, but not neuronal c‐Fos.ConclusionsThese results find acute EtOH combined with acute stress enhanced plasma endotoxin, as well as microglial CD11b in many brain regions. Chronic EtOH followed by acute stress also increased plasma endotoxin and microglial CD11b, suggesting a lasting sensitization to acute stress. Overall, these data suggest alcohol and stress interact to increase plasma endotoxin, resulting in enhanced microglial activation that could contribute to disease progression.

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“…Approximately 65 cubic angstroms of molecular volume is lost when phenylalanine is replaced by cysteine (Vilpoux et al, 2009), whereas covalently linking propyl or pentyl-MTS to cysteine increases volume by approximately 102 and 140 cubic angstroms, respectively. Similarly, in previous studies, replacing GluN1 F639 with larger residues such as tryptophan (Ronald et al, 2001) or tyrosine ) enhances or does not change ethanol inhibition, suggesting that TM3 639 accommodates large side chain volumes with little change in receptor function or ethanol inhibition.…”

Section: Discussionmentioning

confidence: 99%

Cysteine Substitution of Transmembrane Domain Amino Acids Alters the Ethanol Inhibition of GluN1/GluN2A N-Methyl-d-Aspartate Receptors

Smothers

Woodward

2015

J Pharmacol Exp Ther

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N-Methyl-D-aspartate receptors (NMDARs) are inhibited by behaviorally relevant concentrations of ethanol, and residues within transmembrane (TM) domains of NMDARs, including TM3 GluN1 phenylalanine 639 (F639), regulate this sensitivity. In the present study, we used cysteine (C) mutagenesis to determine whether there are additional residues within nearby TM domains that regulate ethanol inhibition on NMDARs. GluN1(F639C)/GluN2A receptors were less inhibited by ethanol than wild-type receptors, and inhibition was restored to wild-type levels following treatment with ethanol-like methanethiosulfonate reagents. Molecular modeling identified six residues in the GluN1 TM1 domain (valine V566; serine S569) and the GluN2A TM4 domain (methionine, M817; V820, F821, and leucine, L824) that were in close vicinity to the TM3 F639 residue, and these were individually mutated to cysteine and tested for ethanol inhibition and receptor function. The F639C-induced decrease in ethanol inhibition was blunted by coexpression of GluN1 TM1 mutants V566C and S569C, and statistically significant interactions were observed for ethanol inhibition among V566C, F639C, and GluN2A TM4 mutants V820C and F821C and S569C, F639C, and GluN2A TM4 mutants F821C and L824C. Ethanol inhibition was also reduced when either GluN1 TM1 mutant V566C or S569C was combined with GluN2A V820C, suggesting a novel TM1:TM4 intrasubunit site of action for ethanol. Cysteines substituted at TM3 and TM4 sites previously suggested to interact with ethanol had less dramatic effects on ethanol inhibition. Overall, the results from these studies suggest that interactions among TM1, TM3, and TM4 amino acids in NMDARs are important determinants of ethanol action at these receptors.

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Ethanol‐Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression

Abstract: A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies.

Cited by 115 publications

References 143 publications

Repeated Binge-Like Ethanol Administration During Adolescence cause Decreased C-Fos Immunoreactivity in Amygdala and Arcuate Nucleus in Adult Sprague-Dawley Rats

Repeated Binge-Like Ethanol Administration During Adolescence cause Decreased C-Fos Immunoreactivity in Amygdala and Arcuate Nucleus in Adult Sprague-Dawley Rats

Alcohol and Stress Activation of Microglia and Neurons: Brain Regional Effects

Cysteine Substitution of Transmembrane Domain Amino Acids Alters the Ethanol Inhibition of GluN1/GluN2A N-Methyl-d-Aspartate Receptors

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