Alcohol-induced conditioned place preference negatively correlates with anxiety-like behavior in adolescent mice: inhibition by a neurokinin-1 receptor antagonist

Huang, Hui; Zhang, Xiaojie; Fu, Xiaoya; Zhang, Xiangyang; Luo, Bing; Xiang, Xiaojun; Hao, Wei

doi:10.1007/s00213-018-4976-7

Cited by 7 publications

(5 citation statements)

References 65 publications

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“…In fact, and after a period of conditioning, the mice spent significantly more time in the chamber paired with EtOH. These results are consistent with earlier studies, from our laboratory (Al Bahi and Dreyer 2014;Bahi et al 2014b) and from others, in which 2 g kg −1 EtOH elicited a robust CPP in both mice (Huang et al 2018;Marcus et al 2017;Xie et al 2019), and rats (Fu et al 2016;Okhuarobo et al 2018;Zuo et al 2017). Next, we found, in the 1st experiment, that repeated daily exposure to both conditioning chambers successfully extinguished this CPP.…”

Section: Discussionsupporting

confidence: 93%

Environmental enrichment decreases chronic psychosocial stress-impaired extinction and reinstatement of ethanol conditioned place preference in C57BL/6 male mice

Bahí

Dreyer

2019

Psychopharmacology

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Rationale During the last few decades, alcohol use disorders (AUD) have reached an epidemic prevalence, yet social influences on alcoholism have not been fully addressed. Several factors can modulate alcohol intake. On one hand, stress can reinforce ethanol-induced behaviors and be an important component in AUD and alcoholism. On the other hand, environmental enrich-ment (EE) has a neuroprotective role and prevents the development of excessive ethanol intake in rodents. However, studies showing the role of EE in chronic psychosocial stress-impaired ethanol-conditioned rewards are nonexistent. Aim The purpose of the current study is to explore the potential protective role of EE on extinction and reinstatement of ethanolconditioned place preference (EtOH-CPP) following chronic psychosocial stress. Methods In the first experiment and after the EtOH-CPP test, the mice were subjected to 15 days of chronic stress, then housed in a standard (SE) or enriched environment (EE) while EtOH-CPP extinction was achieved by repeated exposure to the CPP chambers without ethanol injection. In the second experiment and after the EtOH-CPP test, extinction was achieved as described above. Mice were then exposed to chronic stress for 2 weeks before being housed in a SE or EE. EtOH-CPP reinstatement was induced by a single exposure to the conditioning chambers. Results As expected, stress exposure increased anxiety-like behavior and reduced weight gain. More importantly, we found that EE significantly shortened chronic stress-delayed extinction and decreased the reinstatement of EtOH-CPP. Conclusion These results support the hypothesis that EE reduces the impact of alcohol-associated environmental stimuli, and hence it may be a general intervention for reducing cue-elicited craving and relapse in humans.

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Section: Discussionsupporting

confidence: 93%

Environmental enrichment decreases chronic psychosocial stress-impaired extinction and reinstatement of ethanol conditioned place preference in C57BL/6 male mice

Bahí

Dreyer

2019

Psychopharmacology

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“…Over 35 generations later, bHR and bLR rats exhibited all of the key features of the outbred HR/LR rats while also exhibiting correlated differences in low anxiety‐like, or risk‐taking behaviors during EPM, LDB, and OFA paradigms 17 . Analogous to the HR/LR rat lines, Huang et al 19 used the EPM to assess the anxiety‐like behavior of C57BL/6J mice and afterwards separated the mice into HAM and LAM groups. Finally, similar to the bHR/bLR rat lines, Krömer et al 18 created a high (HAB), normal (NAB), and low (LAB) anxiety‐related behavior mouse model by selectively inbreeding outbred CD‐1 mice based on their behavior in the EPM for over 15 generations.…”

Section: Discussionmentioning

confidence: 99%

“…17 Additionally, Krömer et al 18 utilized the EPM to create CD-1 mouse models of high (HAB), normal (NAB), and low (LAB) anxiety behaviors. Finally, Huang et al 19 performed a similar paradigm to create C57BL/6J high (HAM) and low (LAM) anxiety mouse models.…”

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confidence: 99%

Anxiety‐related defensive behavioral responses in mice selectively bred for High and Low Activity

Booher

Hall

Thomas

et al. 2021

Genes Brain and Behavior

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High and Low Activity strains of mice (displaying low and high anxiety-like behavior, respectively) with 7.8-20 fold differences in open-field activity were selected and subsequently inbred to use as a genetic model for studying anxiety-like behavior in mice (DeFries et al., 1978, Behavior Genetics, 8:3-13). These strains exhibited differences in other anxiety-related behaviors as assessed using the light-dark box, elevated plus-maze, mirror chamber, and elevated square-maze tests (Henderson et al., 2004, Behavior Genetics, 34: 267-293). The purpose of these experiments was three-fold. First, we repeated a 6-day behavioral battery using updated equipment

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“…In addition, Ribeiro and De Lima (2002) demonstrated that NKR2 antagonists can block the anxiogenic effects of pentylenetetrazol. Combined, these data may suggest a role for NKRs in anxiety and alcohol reward in adolescent mice (Huang et al, 2018) that may also be important in this rat model of adolescent binge drinking.…”

Section: Discussionmentioning

confidence: 88%

“…Tachykinin receptors (TACR2, TACR3) encode for tachykinin neuropeptide substance K (NK2 and NK3). Huang et al (2018) showed that low-anxiety mice have a greater preference for ethanol when compared to the high-anxiety mouse group. Low-anxiety mice also had higher levels of NK1 receptor (NKR1) in the hippocampus when compared to the high-anxiety group.…”

Section: Addictionmentioning

confidence: 99%

Comparative gene pathway analysis during adolescent binge-EtOH exposure, withdrawal, and following abstinence

Nato

Mustafa

Patel

et al. 2020

Preprint

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Introduction: Alcohol use disorder (AUD) is a complex, chronic psychiatric disease. AUD manifests as having uncontrollable drinking patterns with detrimental effects. Excessive alcohol intake in the form of binge drinking, which is common among adolescents and young adults, is associated with increased risk of developing AUD. Here, we analyze RNA-seq data from hippocampi of Sprague Dawley rats to investigate temporal changes in gene expression. We used a rodent model of binge drinking, i.e., adolescent intermittent ethanol (AIE), to identify candidate genes that may play a role in the chronic changes in brain function and contribute to the development of AUD. Methods: At postnatal day (PND) 30 (adolescence), rats received chronic intermittent ethanol (5g/kg intragastrically (i.g.) 10 times across 16 days). We extracted total RNA from rat hippocampal tissue that was collected at three time points. RNA was sequenced on an Illumina HiSeq 2000 platform. We processed RNA-seq data (TrimGalore), compiled gene counts (HTSeq), and performed differential expression analysis (DESeq2). The full rank list of genes and the differentially expressed genes (DEGs) with nominal p<0.05 were used as inputs for pathway-based enrichment analyses GSEA and Cytoscape, respectively, at 3 timepoints in the presence or absence of ethanol (i.e., 3 comparisons). For each of these comparisons, GSEA was used to identify genes involved in enriched Gene Ontology (GO) terms while Cytoscape and its apps were used to identify networks of genes and, subsequently, subnetworks (i.e., clusters) of genes enriched by higher interaction. From clusters containing 15 or more nodes, we prioritized genes related with particular functions, cell types, or diseases, which were present in GO Processes, Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathways, or Reactome Pathways. Results: Based on GSEA, the most impacted differential gene expression occurs within the potassium channels and receptor function but is heavily dependent on the time point at which the analysis occurs. Across both GSEA and Cytoscape pathway analyses, the most striking changes occur in genes that regulate neuroinflammatory processes and neuronal/synaptic remodeling and coincide with the enrichment of pathways involved in addiction processes. Conclusion: Identification of genes dysregulated by AIE may be useful in determining the underlying mechanism for acute and chronic effects of AIE exposure that contribute to neuronal remodeling and increased risk of developing AUD.

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Alcohol-induced conditioned place preference negatively correlates with anxiety-like behavior in adolescent mice: inhibition by a neurokinin-1 receptor antagonist

Cited by 7 publications

References 65 publications

Environmental enrichment decreases chronic psychosocial stress-impaired extinction and reinstatement of ethanol conditioned place preference in C57BL/6 male mice

Environmental enrichment decreases chronic psychosocial stress-impaired extinction and reinstatement of ethanol conditioned place preference in C57BL/6 male mice

Anxiety‐related defensive behavioral responses in mice selectively bred for High and Low Activity

Comparative gene pathway analysis during adolescent binge-EtOH exposure, withdrawal, and following abstinence

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