ArticleAlcoholism, clinical and experimental research2018
Glyoxalase 1 (GLO1) Inhibition or Genetic Overexpression Does Not Alter Ethanol's Locomotor Effects: Implications for GLO1 as a Therapeutic Target in Alcohol Use Disorders.
Article in Alcoholism, clinical and experimental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Cyp2e1 deletion in mice increases sensitivity to ethanol-induced motor impairment and escalation of drinking behavior in the chronic intermittent ethanol model.Alcohol, clinical & experimental research · 2025Article
- Pharmacological and genetic manipulation of glyoxalase-1 (GLO1) does not alter locomotor responses or conditioned place preference induced by cocaine or oxycodone.Pharmacology, biochemistry, and behavior · 2025Article
- Methylglyoxal in the Brain: From Glycolytic Metabolite to Signalling Molecule.Molecules (Basel, Switzerland) · 2022Review
- A mutant allele of glycoprotein M6-B (Gpm6b) facilitates behavioral flexibility but increases delay discounting.Genes, brain, and behavior · 2022Article
- Fentanyl-induced acute and conditioned behaviors in two inbred mouse lines: Potential role for Glyoxalase.Physiology & behavior · 2022Article
- Inhibition of Glyoxalase 1 reduces alcohol self-administration in dependent and nondependent rats.Pharmacology, biochemistry, and behavior · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGlyoxalase 1 (GLO1) is an enzyme that metabolizes methylglyoxal (MG), which is a competitive partial agonist at GABA
methodsMale C57BL/6J mice were pretreated with either the GLO1 inhibitor S-bromobenzylglutathione cyclopentyl diester (pBBG; 7.5 mg/kg; Experiment 1) or muscimol (0.75 mg/kg; Experiment 2), or their corresponding vehicle. We then determined whether locomotor response to a range of EtOH doses (0, 0.5, 1.0, 1.5, 2.0, and 2.5) was altered by either pBBG or muscimol pretreatment. We also examined the locomotor response to a range of EtOH doses in FVB/NJ wild-type and transgenic Glo1 overexpressing mice (Experiment 3). Anxiety-like behavior (time spent in the center of the open field) was assessed in all 3 experiments.
resultsThe EtOH dose-response curve was not altered by pretreatment with pBBG or by transgenic overexpression of Glo1. In contrast, muscimol blunted locomotor stimulation at low EtOH doses and potentiated locomotor sedation at higher EtOH doses. No drug or genotype differences were seen in anxiety-like behavior after EtOH treatment.
conclusionsThe dose of pBBG used in this study is within the effective range shown previously to reduce EtOH drinking. Glo1 overexpression has been previously shown to increase EtOH drinking. However, neither manipulation altered the dose-response curve for EtOH's locomotor effects, whereas muscimol appeared to enhance the locomotor sedative effects of EtOH. The present data demonstrate that reduced EtOH drinking caused by GLO1 inhibition is not due to potentiation of EtOH's stimulant or depressant effects.
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