ArticleGenes, brain, and behavior2014
Sex-specific behavioral traits in the Brd2 mouse model of juvenile myoclonic epilepsy.
Article in Genes, brain, and behavior, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Transcriptomic Challenges We Faced with Animal Models for Neurological Disorders.Current issues in molecular biology · 2026Review
- Effects of Sildenafil on Cognitive Function Recovery and Neuronal Cell Death Protection after Transient Global Cerebral Ischemia in Gerbils.Biomedicines · 2024Article
- Variants in BRWD3 associated with X-linked partial epilepsy without intellectual disability.CNS neuroscience & therapeutics · 2023Article
- Alterations of the intrinsic amygdala-hippocampal network in juvenile myoclonic epilepsy.Brain and behavior · 2021Article
- BET bromodomains as novel epigenetic targets for brain health and disease.Neuropharmacology · 2020Review
- Sex Differences in the Epilepsies and Associated Comorbidities: Implications for Use and Development of Pharmacotherapies.Pharmacological reviews · 2020Review
- Modeling epileptic spasms during infancy: Are we heading for the treatment yet?Pharmacology & therapeutics · 2020Review
- Article
- Progranulin haploinsufficiency causes biphasic social dominance abnormalities in the tube test.Genes, brain, and behavior · 2016Article
- Genetic absence of nNOS worsens fetal alcohol effects in mice. I: behavioral deficits.Alcoholism, clinical and experimental research · 2015Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Idiopathic generalized epilepsy represents about 30-35% of all epilepsies in humans. The bromodomain BRD2 gene has been repeatedly associated with the subsyndrome of juvenile myoclonic epilepsy (JME). Our previous work determined that mice haploinsufficient in Brd2 (Brd2+/-) have increased susceptibility to provoked seizures, develop spontaneous seizures and have significantly decreased gamma-aminobutyric acid (GABA) markers in the direct basal ganglia pathway as well as in the neocortex and superior colliculus. Here, we tested male and female Brd2+/- and wild-type littermate mice in a battery of behavioral tests (open field, tube dominance test, elevated plus maze, Morris water maze and Barnes maze) to identify whether Brd2 haploinsufficiency is associated with the human behavioral patterns, the so-called JME personality. Brd2+/- females but not males consistently displayed decreased anxiety. Furthermore, we found a highly significant dominance trait (aggression) in the Brd2+/- mice compared with the wild type, more pronounced in females. Brd2+/- mice of either sex did not differ from wild-type mice in spatial learning and memory tests. Compared with wild-type littermates, we found decreased numbers of GABA neurons in the basolateral amygdala, which is consistent with the increase in aggressive behavior. Our results indicate that Brd2+/- haploinsufficient mice show no cognitive impairment but have behavioral traits similar to those found in patients with JME (recklessness, aggression). This suggests that either the BRD2 gene is directly responsible for influencing many traits of JME or it controls upstream regulators of individual phenotypes.
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