ArticlePLoS genetics2015
TSPO, a Mitochondrial Outer Membrane Protein, Controls Ethanol-Related Behaviors in Drosophila.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- From Natural Behavior to Drug Screening: Invertebrates as Models to Study Mechanisms Associated with Alcohol Use Disorders.Current topics in behavioral neurosciences · 2025Review
- Large analysis of genetic manipulations reveals an inverse correlation between initial alcohol resistance and rapid tolerance phenotypes.Genes, brain, and behavior · 2024Article
- Large genetic analysis of alcohol resistance and tolerance reveals an inverse correlation and suggests 'true' tolerance mutants.bioRxiv : the preprint server for biology · 2023Article
- Increased transcription of TSPO, HDAC2, and HDAC6 in the amygdala of males with alcohol use disorder.Brain and behavior · 2021Article
- Review
- Review
- Translocator Protein Ligand Protects against Neurodegeneration in the MPTP Mouse Model of Parkinsonism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Influence of alcoholism and cholesterol on TSPO binding in brain: PET [Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Sex-dependent mental illnesses and mitochondria.Schizophrenia research · 2017Review
- Genetics and genomics of alcohol responses in Drosophila.Neuropharmacology · 2017Review
- SlgA, encoded by the homolog of the human schizophrenia-associated geneDisease models & mechanisms · 2017Article
- α-amanitin resistance in Drosophila melanogaster: A genome-wide association approach.PloS one · 2017Article
- Interactions between inflammation, sex steroids, and Alzheimer's disease risk factors.Frontiers in neuroendocrinology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The heavy consumption of ethanol can lead to alcohol use disorders (AUDs) which impact patients, their families, and societies. Yet the genetic and physiological factors that predispose humans to AUDs remain unclear. One hypothesis is that alterations in mitochondrial function modulate neuronal sensitivity to ethanol exposure. Using Drosophila genetics we report that inactivation of the mitochondrial outer membrane translocator protein 18kDa (TSPO), also known as the peripheral benzodiazepine receptor, affects ethanol sedation and tolerance in male flies. Knockdown of dTSPO in adult male neurons results in increased sensitivity to ethanol sedation, and this effect requires the dTSPO depletion-mediated increase in reactive oxygen species (ROS) production and inhibition of caspase activity in fly heads. Systemic loss of dTSPO in male flies blocks the development of tolerance to repeated ethanol exposures, an effect that is not seen when dTSPO is only inactivated in neurons. Female flies are naturally more sensitive to ethanol than males, and female fly heads have strikingly lower levels of dTSPO mRNA than males. Hence, mitochondrial TSPO function plays an important role in ethanol sensitivity and tolerance. Since a large array of benzodiazepine analogues have been developed that interact with the peripheral benzodiazepine receptor, the mitochondrial TSPO might provide an important new target for treating AUDs.
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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.