GABRQ

Last update 08 May 2025

Basic Info

Synonyms

GABA(A) receptor subunit theta, GABA(A) receptor, theta, GABRQ

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Introduction

Theta subunit of the heteropentameric ligand-gated chloride channel gated by gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain (PubMed:10449790, PubMed:16412217). GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interfaces (By similarity). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient (PubMed:10449790, PubMed:16412217).

100 Clinical Results associated with GABRQ

100 Translational Medicine associated with GABRQ

0 Patents (Medical) associated with GABRQ

Literatures (Medical) associated with GABRQ

01 Jun 2025·Neurobiology of Disease

Disrupted synaptic gene expression in Fabry disease: Findings from RNA sequencing

Article

Author: Villacorta-Argüelles, Eduardo ; Leao-Teles, Elisa ; López, Lluis Lis ; Álvarez, J Víctor ; López-Valverde, Laura ; Hermida-Ameijeiras, Álvaro ; Couce, María L ; Vázquez-Mosquera, María E ; Colón-Mejeras, Cristóbal ; López-Mendoza, Manuel ; López-Pardo, Beatriz Martín ; López-Rodríguez, Mónica ; Goicoechea-Diezhandino, María A ; Ortolano, Saida ; Sánchez-Martínez, Rosario ; Guerrero-Márquez, Francisco J

Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by a deficiency in the enzyme α-galactosidase A. This defect leads to the progressive accumulation of glycosphingolipids, resulting in kidney, heart, and nervous system damage, which contributes to significant morbidity and mortality. Early diagnosis is essential to prevent irreversible damage and optimize treatment strategies. Recent research aims to provide a better understanding of FD pathophysiology to improve management approaches. This study is an international, multicenter, cross-sectional analysis that used RNA sequencing (RNA-seq) to compare blood samples from 50 FD patients and 50 age- and sex-matched healthy controls. The objective was to identify gene expression patterns and investigate secondary cellular pathways affected by lysosomal dysfunction. Among the more than 400 differentially expressed genes detected, 207 were protein-coding genes, most of which were overexpressed in the FD cohort. Functional enrichment analysis highlighted processes related to synaptic function, specifically concerning chemical synaptic transmission and membrane potential regulation. Identified genes included those related to voltage-gated ion channels, neurotransmitter receptors, cell adhesion molecules, scaffold proteins, and proteins associated with synaptic vesicles and neurotrophic signaling, all linked to lipid rafts. Notable identified genes included those encoding voltage-gated potassium channel genes (KCNQ2, KCNQ3, KCNMA1) and ionotropic receptor genes involved in glutamatergic (GRIN2A, GRIN2B) and GABAergic systems (GABRA4, GABRB1, GABRG2, GABRQ). These findings suggest that lysosomal dysfunction contributes to synaptic defects in FD, paving the way for further research into the role of synaptic pathology and lipid rafts in the underlying pathogenesis and clinical outcomes in FD.

01 May 2023·Phytotherapy Research

Proteomic and metabolomic approaches elucidate the molecular mechanism of emodin against neuropathic pain through modulating the gamma‐aminobutyric acid (GABA)‐ergic pathway and PI3K/AKT/NF‐κB pathway

Article

Author: Luo, Rui‐xi ; Chen, Peng ; Wang, Chen ; Huang, Ning‐yu ; Pang, Bo ; Gong, Qian ; Ye, Zeng‐jie ; Liu, Chang ; Wang, Long

AbstractNeuropathic pain (NeP) is a major health concern. Due to the complex pathological mechanisms, management of NeP is challenging. Emodin, a natural anthraquinone derivative, exerts excellent analgesic effects. However, its mechanisms of action are still poorly understood. In this study, we investigated the mechanisms underlying pain‐relief effects of emodin in the cerebral cortex using proteomic and metabolomic approaches. After 15 days of emodin administration, the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) values in the emodin groups were significantly higher than those in the chronic constriction injury (CCI) group (p < .05), suggesting emodin treatment could reverse CCI‐induced hyperalgesia. Emodin treatment evoked the expression alteration of 402 proteins (153 up‐regulated and 249 down‐regulated) in the CCI models, which were primarily involved in PI3K/AKT signaling pathway, gamma‐aminobutyric acid (GABA) receptor signaling, complement and coagulation cascades, cGMP/PKG signaling pathway, MAPK signaling pathway, and calcium signaling pathway. In parallel, emodin intervention regulated the abundance alteration of 27 brain metabolites (20 up‐regulated and 7 down‐regulated) in the CCI rats, which were primarily implicated in carbon metabolism, biosynthesis of amino acids, pentose phosphate pathway, and glucagon signaling pathway. After a comprehensive analysis and western blot validation, we demonstrated that emodin alleviated NeP mainly through regulating GABAergic pathway and PI3K/AKT/NF‐κB pathway.

01 Feb 2023·Neurogastroenterology & Motility

Regulation of the central amygdala on intestinal motility and behavior via the lateral hypothalamus in irritable bowel syndrome model mice

Article

Author: Chen, Ziyi ; Gao, Shengli ; Ming, Xing ; Ji, Pengfei ; Guo, Feifei ; Guo, Ruixiao ; Yu, Lizheng ; He, Xiaoman ; Zhang, Hongfei

AbstractBackgroundImpaired bidirectional communication between the gastrointestinal tract and the central nervous system (CNS) is closely related to the development of irritable bowel syndrome (IBS). Studies in patients with IBS have also shown significant activation of the hypothalamus and amygdala. However, how neural circuits of the CNS participate in and process the emotional and intestinal disorders of IBS remains unclear.MethodsThe GABAergic neural pathway projecting from the central amygdala (CeA) to the lateral hypothalamus (LHA) in mice was investigated by retrograde tracking combined with fluorescence immunohistochemistry. Anxiety, depression‐like behavior, and intestinal motility were observed in the water‐immersion restraint stress group and the control group. Furthermore, the effects of the chemogenetic activation of the GABAergic neural pathway of CeA‐LHA on behavior and intestinal motility, as well as the co‐expression of orexin‐A and c‐Fos in the LHA, were explored.Key ResultsIn our study, Fluoro‐Gold retrograde tracking combined with fluorescence immunohistochemistry showed that GABAergic neurons in the CeA were projected to the LHA. The microinjection of the gamma‐aminobutyric acid (GABA) receptor antagonist into the LHA relieved anxiety, depression‐like behavior, and intestinal motility disorder in the IBS mice. The chemogenetic activation of GABAergic neurons in the CeA‐LHA pathway led to anxiety, depression‐like behavior, and intestinal motility disorder. In addition, GABAergic neurons in the CeA‐LHA pathway inhibited the expression of orexin‐A in the LHA, and orexin‐A was co‐expressed with GABAA receptors.Conclusions & InferencesThe CeA‐LHA GABAergic pathway might participate in the occurrence and development of IBS by regulating orexin‐A neurons.

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GABRQ

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