GABAB Receptor 1 Antibody, Clone N93A/49: RPE

GABA (γ-aminobutyric acid) is the brain’s primary inhibitory neurotransmitter, acting through three receptor types: GABA-A, GABA-B, and GABA-C. While GABA-A and GABA-C receptors are ionotropic and mediate fast synaptic inhibition, GABA-B receptors are metabotropic, G protein-coupled receptors that regulate slow, prolonged inhibitory signaling. The functional GABA-B receptor is a heterodimer composed of GABA-B Receptor 1 (GABBR1), which binds the ligand, and GABA-B Receptor 2 (GABBR2), which couples to intracellular G proteins. GABBR1 exists in two isoforms—GABBR1a and GABBR1b—each contributing to distinct signaling dynamics. Upon activation, GABA-B receptors inhibit adenylate cyclase, reduce calcium influx at presynaptic terminals, and activate inwardly rectifying potassium channels postsynaptically, thereby modulating neurotransmitter release and neuronal excitability. GABBR1 plays a critical role in maintaining synaptic balance and has been implicated in key neurological processes such as hippocampal long-term potentiation, slow-wave sleep, and motor control. Importantly, dysregulation of GABA-B signaling—particularly involving GABBR1—has been linked to neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Altered GABBR1 expression or function may contribute to excitotoxicity, impaired synaptic plasticity, and cognitive decline. As a result, GABBR1 is emerging as a promising therapeutic target and biomarker in neurodegeneration research, offering new avenues for modulating inhibitory tone and preserving neural function in aging and disease.

1 µg/ml of SMC-403 was sufficient for detection of GABA (B) R1 in 20 µg of rat brain membrane lysate and assayed by colorimetric immunoblot analysis using goat anti-mouse IgG:HRP as the secondary antibody.

1. Jones K.A,. et al. (2000) Neuropsychopharmacology 23: S41-9. 2. Duthey B., et al. (2002) J Biol Chem. 277: 3236-41. 3. Kaupmann K., et al. (1997) Nature 386: 239-46.

1. Jones K.A, . et al. (2000) Neuropsychopharmacology 23: S41-9. 2. Duthey B., et al. (2002) J Biol Chem. 277: 3236-41. 3. Kaupmann K., et al. (1997) Nature 386: 239-46.