ArticleNeuropharmacology2016
Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice.
Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- Alcohol drinking sex-dependently regulates interleukin-1 pro-inflammatory signaling in the prefrontal cortex of mice and rhesus macaques.Brain, behavior, and immunity · 2026Article
- Chronic alcohol consumption sex-dependently affects IL-6 modulation of GABAergic synapses in the central amygdala of rhesus macaques.Brain, behavior, and immunity · 2026Article
- Article
- Chronic ethanol induces a pro-inflammatory switch in interleukin-1β regulation of GABAergic signaling in the medial prefrontal cortex of male mice.Brain, behavior, and immunity · 2023Article
- Chronic ethanol alters adrenergic receptor gene expression and produces cognitive deficits in male mice.Neurobiology of stress · 2023Article
- Astrocytes play a critical role in mediating the effect of acute ethanol on central amygdala glutamatergic transmission.Neuropharmacology · 2022Article
- Subregional Differences in Alcohol Modulation of Central Amygdala Neurocircuitry.Frontiers in molecular neuroscience · 2022Review
- Aberrant role of ALK in tau proteinopathy through autophagosomal dysregulation.Molecular psychiatry · 2021Article
- Opioid System Contributes to the Trifluoromethyl-Substituted Diselenide Effectiveness in a Lifestyle-Induced Depression Mouse Model.Molecular neurobiology · 2021Article
- Binge-like ethanol drinking activates anaplastic lymphoma kinase signaling and increases the expression of STAT3 target genes in the mouse hippocampus and prefrontal cortex.Genes, brain, and behavior · 2021Article
- The escalation in ethanol consumption following chronic intermittent ethanol exposure is blunted in mice expressing ethanol-resistant GluN1 or GluN2A NMDA receptor subunits.Psychopharmacology · 2021Article
- Growth Factors and Alcohol Use Disorder.Cold Spring Harbor perspectives in medicine · 2020Review
- Leveraging Neural Networks in Preclinical Alcohol Research.Brain sciences · 2020Review
- Male-specific association of the 2p25 region with suicide attempt in bipolar disorder.Journal of psychiatric research · 2020Article
- Receptor Tyrosine Kinases as Therapeutic Targets for Alcohol Use Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Article
- Driving the Downward Spiral: Alcohol-Induced Dysregulation of Extended Amygdala Circuits and Negative Affect.Alcoholism, clinical and experimental research · 2019Review
- Morphological and functional evidence of increased excitatory signaling in the prelimbic cortex during ethanol withdrawal.Neuropharmacology · 2018Article
- Genetics and genomics of alcohol responses in Drosophila.Neuropharmacology · 2017Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that is expressed in the brain and implicated in alcohol abuse in humans and behavioral responses to ethanol in mice. Previous studies have shown an association of human ALK with acute responses to alcohol and alcohol dependence. In addition, Alk knockout (Alk -/-) mice consume more ethanol in a binge-drinking test and show increased sensitivity to ethanol sedation. However, the function of ALK in excessive drinking following the establishment of ethanol dependence has not been examined. In this study, we tested Alk -/- mice for dependence-induced drinking using the chronic intermittent ethanol-two bottle choice drinking (CIE-2BC) protocol. We found that Alk -/- mice initially consume more ethanol prior to CIE exposure, but do not escalate ethanol consumption after exposure, suggesting that ALK may promote the escalation of drinking after ethanol dependence. To determine the mechanism(s) responsible for this behavioral phenotype we used an electrophysiological approach to examine GABA neurotransmission in the central nucleus of the amygdala (CeA), a brain region that regulates alcohol consumption and shows increased GABA signaling after chronic ethanol exposure. GABA transmission in ethanol-naïve Alk -/- mice was enhanced at baseline and potentiated in response to acute ethanol application when compared to wild-type (Alk +/+) mice. Moreover, basal GABA transmission was not elevated by CIE exposure in Alk -/- mice as it was in Alk +/+ mice. These data suggest that ALK plays a role in dependence-induced drinking and the regulation of presynaptic GABA release in the CeA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.