Ask about this productRelated genes to: GABRA1 Blocking Peptide
- Gene:
- GABRA1 NIH gene
- Name:
- gamma-aminobutyric acid type A receptor alpha1 subunit
- Previous symbol:
- -
- Synonyms:
- EJM5
- Chromosome:
- 5q34
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-02
- Date modifiied:
- 2016-02-04
Related products to: GABRA1 Blocking Peptide
Related articles to: GABRA1 Blocking Peptide
- Sleep deprivation (SD) is associated with anxiety-like behaviors, yet the underlying molecular and neural circuit mechanisms remain unclear. Using a 24-hour SD paradigm in mice, we found that SD induced anxiety-like behaviors and increased interleukin-6 (IL-6) in blood and the periaqueductal gray (PAG), and PAG-targeted administration of IL-6 receptor antagonist rescued the anxiety-like behaviors. This increased IL-6 activated PAG astrocytes, as evidenced by morphological remodeling, increased calcium activity, and enhanced glutamate release. Astrocytic activation upregulated several genes associated with endoplasmic reticulum (ER) protein synthesis and processing, including neuronal mesencephalic astrocyte-derived neurotrophic factor (Manf). Knockdown of Manf in PAG neurons upregulated the GABA receptor α1 subunit (Gabra1), reduced the activity of GABAergic neurons projecting to the anterior cingulate cortex (ACC), and rescued anxiety-like behaviors. Chemogenetic inhibition of this PAG-ACC circuit prevented SD-induced anxiety-like behaviors, whereas its activation recapitulated the anxiety-like behaviors. Our study identifies an IL-6-astrocyte-Manf signaling axis in the PAG that drives anxiety-like behaviors via enhanced GABAergic neuronal output to the ACC. This PAG-ACC circuit may serve as a neuroimmune hub for SD-mediated anxiety-like behaviors and represents a potential therapeutic target. - Source: PubMed
Publication date: 2026/05/22
Xu XiaoWu ZiangHang WenxinMao ShaojiaSun JiahuiXiong HuanbinZhu JinpiaoMa Daqing - Anxiety is a common non-motor symptom of Parkinson's disease (PD), affecting 20 %-50 % of the patients, with an unmet need for effective therapies. Although perineuronal net (PNN) abnormalities have been implicated in both PD and anxiety, the underlying mechanisms and potential treatments remain poorly characterised. - Source: PubMed
Publication date: 2026/05/07
Dong YixiaoZhang XinyueZhou XinleZhao KunkunYang XinaLi QianwenDu GuanhuaGao Li - Late-life depression (LLD) is a debilitating condition, characterized by mood disturbance and cognitive decline. Gamma-aminobutyric acidergic (GABAergic) deficits are a hallmark of both aging and depression; however, few studies have examined the GABAergic system in LLD. We hypothesized that there would be significant decrease in peripheral GABA levels and γ-aminobutyric acid type A (GABA-A) receptor subunit expression in individuals with LLD compared to healthy controls (HC). In this study, we measured plasma GABA levels and the mRNA expression of four GABA-A receptor subunits (GABRA1, GABRA4, GABRA5, and GABRR2) in peripheral blood mononuclear cells (PBMCs) from 87 older adults (LLD, n = 46; HC, n = 41). Plasma GABA levels were quantified using enzyme-linked immunosorbent assay (ELISA), and receptor subunit expression was assessed by quantitative-real time (RT-qPCR). There were no significant differences between LLD and HC in plasma GABA levels or GABA-A receptor subunit expression. In LLD, within-group analyses showed GABRA5, GABRR2, GABRA4, GABRA1 expression were negatively correlated with cognitive performance on the Montreal Cognitive Assessment MoCA scores (ρ = -0.464, p = 0.045, ρ = -0.515, p = 0.041; ρ = -0.414, p = 0.078, and ρ = -0.477, p = 0.062 respectively). This is the first study that investigated GABA-A receptor subunit expression in the periphery of individuals with LLD. Our findings suggest that altered peripheral GABA-A receptor subunit expression, even in the absence of between-group differences, is associated with reduced cognitive function in LLD. - Source: PubMed
Publication date: 2026/05/03
Rezaei SaraSibille EtienneVoineskos DaphneRajji Tarek KNikolova Yuliya SDiniz Breno SVieira Erica L - Glioblastoma recurrence is driven by diffuse microscopic infiltration beyond the contrast-enhancing tumour margin. GlioMap is an open-access AI model predicting voxelwise infiltration and recurrence risk from multiparametric MRI. This prospective study aimed to validate GlioMap's biological accuracy and prognostic relevance through histopathological assessment, transcriptomic profiling, and survival analysis within the SupraGlio trial (NCT05735171). - Source: PubMed
Publication date: 2026/04/20
Cepeda SantiagoHernando-Pérez ElenaPérez-Riesgo EnriqueRodríguez-Valle IsabelEsteban-Sinovas OlgaArrese IgnacioLucero-Salaverry María MiguelZamora TomásTorres-Nieto María ÁngelesLuppino Luigi TommasoKuttner SamuelWodzinski MarekEscudero TrinidadGarzón JesúsRomero-Oraá RobertoHornero RobertoNúñez LucíaVillalobos CarlosSarabia Rosario - We investigated whether a water extract of ( Thunberg; WELB) could modulate inhibitory synaptic organization in a mouse model of pentylenetetrazol (PTZ)-induced kindling. Starting 14 days prior to the initial PTZ challenge, WELB (500 mg/kg) was delivered via oral gavage once daily. This treatment regimen was maintained for a total of 40 days, spanning the entire period until the animals reached the fully kindled state. Behavioral assessments revealed that WELB treatment significantly reduced seizure severity and Racine scores, prolonged the latency to clonic seizures, and shortened seizure duration, demonstrating potent anticonvulsant activity. Two-photon calcium imaging further showed that WELB markedly suppressed PTZ-induced neuronal hyperexcitability in the posterior parietal cortex, accompanied by decreased expression of neuronal activation markers, including c-fos, phosphorylated-calcium/calmodulin-dependent protein kinase IIα (p-CaMKIIα), and N-methyl-D-aspartate receptor 1 (NR1). In the hippocampus, WELB modulated the expression of GABAergic interneuron markers [glutamate decarboxylase 67 (GAD67), vesicular GABA transporter (VGAT), parvalbumin (PV), somatostatin (SOM)] and upregulated GABAergic gene transcripts [GABA-A receptor α1 subunit (Gabra1), GABA-A receptor α2 subunit (Gabra2), GABA transporter 1 (Gat1), GABA transporter 3 (Gat3), PV, SOM, cholecystokinin (CCK)] that were downregulated by PTZ kindling. Moreover, WELB enhanced the expression of GABAergic synaptic organization-related proteins (gephyrin, collybistin, neurexin-1β, neuroligin-2, and neuropilin-2), indicating its regulatory effect on inhibitory synaptic integrity. Collectively, these findings suggest that WELB may exert its anticonvulsant effects by functionally remodeling GABAergic synaptic organization-related factors, thereby restoring inhibitory circuit integrity and providing a mechanism-based therapeutic strategy for epilepsy and seizure-related neurological disorders. - Source: PubMed
Publication date: 2026/04/04
Park Hee Ra