Ask about this productRelated genes to: GABRA2 antibody
- Gene:
- GABRA2 NIH gene
- Name:
- gamma-aminobutyric acid type A receptor alpha2 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-02
- Date modifiied:
- 2016-02-04
Related products to: GABRA2 antibody
Related articles to: GABRA2 antibody
- Age-related changes in neurotransmitter systems contribute to declines in cognitive, emotional, and motor function, yet the biological mechanisms linking these changes to aging are not completely understood. Epigenetic regulation offers a promising framework to bridge this gap. DNA methylation-based biomarkers of biological aging (i.e., epigenetic clocks) capture cumulative and dynamic aspects of biological aging that may reflect vulnerability in neural systems beyond chronological age. However, whether these indices track with the integrity of neurotransmitter systems has not been systematically examined. This scoping review synthesizes evidence across human studies to evaluate how epigenetic aging processes influence neurotransmitter gene regulation and system function across the lifespan. We included 109 studies spanning 2005-2026. GABAergic genes (, ) showed the most consistent and reproducible age-related promoter hypermethylation across the cortex, inversely correlated with mRNA expression and corroborated by MRS evidence of cortical GABA decline. Dopaminergic and serotonergic evidence during normative aging was sparse; most epigenetic data in these systems came from disease cohorts. Histone modifications converged on neurotransmission and synaptic-plasticity loci, predominantly in Alzheimer's disease tissue. Subcortical and brainstem nuclei central to monoaminergic and cholinergic systems remain under-investigated for normative aging epigenetic processes. Environmental and social determinants, socioeconomic status, childhood adversity, and chronic stress, were consistently associated with accelerated peripheral epigenetic aging, but brain-specific data are scarce. - Source: PubMed
Publication date: 2026/07/05
Freij Khalid WAkbar ArshiyaDomoyeri PhilemonPolycarp NunayaHigginbotham Dylan RArora ItikaAroke Edwin N - Anxiety is a highly prevalent and disabling comorbidity in autism spectrum disorder (ASD), but its neurobiological mechanisms remain poorly understood. The basolateral amygdala (BLA) is critically involved in anxiety processing, yet the synaptic substrates linking ASD gene mutations to BLA dysfunction are not fully defined. Here, we evaluated anxiety-like behaviors in male Shank3b knockout (Shank3b) mice using open field, elevated plus maze, and light-dark transition tests. Molecular alterations in the BLA were assessed by qPCR and Western blotting, and whole-cell patch-clamp recordings were performed to examine synaptic transmission and intrinsic excitability of BLA pyramidal neurons. Shank3b mice exhibited robust anxiety-like behaviors across multiple behavioral paradigms. In the BLA, expression of the GABA receptor α2 subunit (GABRA2) was significantly reduced, accompanied by decreased levels of NMDA receptor subunits (GluN2A and GluN2B). Electrophysiological recordings revealed a marked reduction in inhibitory synaptic transmission, as evidenced by decreased frequency and amplitude of spontaneous inhibitory postsynaptic currents, whereas excitatory transmission remained largely unchanged, resulting in a significantly elevated excitation/inhibition (E/I) ratio. In addition, BLA pyramidal neurons displayed increased intrinsic excitability, characterized by a depolarized resting membrane potential and enhanced action potential firing. Collectively, these findings identify impaired GABAergic transmission associated with reduced GABRA2 expression as a key mechanism underlying E/I imbalance and heightened neuronal excitability in the BLA of Shank3b-deficient mice, which likely contributes to ASD-related anxiety-like behaviors. These results identify GABA receptor signaling as a promising therapeutic target for pharmacological intervention in ASD-related anxiety. - Source: PubMed
Publication date: 2026/07/13
Li RuitingWang BoRen HuitingAn YananLi XinqianZhang JidongXue QingshengCao Xiaohua - Alcohol use disorder (AUD) is influenced by genetic factors that affect key neurobiological systems, including dopaminergic and GABAergic pathways, which regulate neurobehavioral functions and are modulated by brain-derived neurotrophic factor (BDNF). Variations in these genes contribute to individual vulnerability to AUD. In this study, we investigated single-nucleotide polymorphisms (SNPs) and haplotypic associations in , , and , along with the dopaminergic pathway genes / and , in a Spanish cohort. Peripheral blood-derived genomic DNA was genotyped, and haplotype analyses were conducted. Individual SNPs in , , BDNF, and / showed no significant associations with AUD. In , the rs3219151 T allele was more frequent in AUD patients than in controls (57.9% vs. 49.3%; = 0.03), while the C allele appeared to show a potential protective association. In addition, the GAC haplotype of (rs2197414, rs1992647, rs3219151) was less frequent in AUD than in controls (0.071 vs. 0.122) and showed a protective association (OR = 0.58; 95% CI = 0.34-0.99; = 0.045). Our findings provide exploratory evidence suggesting that specific genetic variants and haplotypes may contribute to AUD susceptibility and support the relevance of multigenic and haplotypic approaches for exploring the neurobiological mechanisms underlying AUD. - Source: PubMed
Publication date: 2026/06/15
Rojas-Pirela MauraGómez Lesmes Sandra PatriciaSalete-Granado DanielLlorente HernánPérez Nieto María-ÁngelesNovo-Veleiro IgnacioCieza-Borrella ClaraPastor IsabelFernández-Mateos JavierInés Revuelta Sandra MChamorro Antonio-JavierLaso Francisco-JavierGonzález-Sarmiento RogelioMarcos Miguel - Gene-environment interactions are thought to contribute to neurodevelopmental psychiatric disorders, yet their behavioral and molecular consequences remain incompletely understood. Here, we examined whether partial deficiency of reelin (Reln) increases susceptibility to a mild prenatal immune challenge in mice. Heterozygous Reln mice and wild-type littermates were exposed to low-dose polyinosinic-polycytidylic acid (Poly(I:C); 2 mg/kg, intraperitoneally) at embryonic day 12.5. Adult male offspring were assessed in the open-field, three-chamber social interaction, and marble-burying tests, followed by gene expression analysis in the medial prefrontal cortex (mPFC). In the open-field test, prenatal Poly(I:C) exposure was associated with increased locomotor activity during the late habituation phase, with the clearest increase in the combined-risk group. In the social interaction test, significant social novelty preference was not detected in the combined-risk group, whereas sociability toward an unfamiliar conspecific was preserved across groups. Marble-burying behavior was reduced in heterozygous Reln mice irrespective of immune challenge, suggesting a genotype-related behavioral alteration that was partly distinct from the combined-risk phenotype observed in the other tests. In the mPFC, several γ-aminobutyric acid A (GABA) receptor subunit transcripts were altered in a gene- and exposure-specific manner. Gabra2 expression was reduced in the combined-risk group, whereas Reln expression was decreased in heterozygous mice independent of immune challenge. These findings indicate that partial Reln deficiency provides a permissive genetic background in which mild prenatal immune activation subtly alters higher-order behavioral adaptation and prefrontal GABA-related gene expression. - Source: PubMed
Iwata KeikoShintani NorihitoMatsuzaki Hideo - The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg