GABBR - Gamma-Aminobutyric Acid B Receptor | Elisa - Clia - Antibody - Protein

Background:

Gamma-Aminobutyric Acid B Receptors (GABBRs) are a class of G protein-coupled receptors (GPCRs) that respond to the neurotransmitter gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. GABBRs were first identified and characterized in the 1980s and 1990s through pharmacological and molecular studies. GABBRs mediate the effects of GABA, leading to inhibition of neurotransmitter release and neuronal excitability. GABBRs are primarily expressed in the central nervous system, particularly in regions involved in synaptic transmission and neuronal excitability, such as the cerebral cortex, hippocampus, basal ganglia, and cerebellum. GABBRs are activated by the neurotransmitter GABA, which binds to the GABBR1 subunit. Several synthetic ligands, including agonists and antagonists, have been developed to selectively modulate GABBR activity for therapeutic purposes.GABBRs play crucial roles in regulating synaptic transmission, neuronal excitability, and synaptic plasticity in the central nervous system. Dysregulation of GABBR signaling is implicated in various neurological and psychiatric disorders

Structural Features:

• Transmembrane Protein: GABBRs are seven-transmembrane domain receptors, typical of GPCRs.
• Topology: They consist of an extracellular N-terminus, seven transmembrane helices connected by intracellular and extracellular loops, and an intracellular C-terminus.
• Heterodimerization: GABBRs typically function as heterodimers composed of GABBR1 (GBR1) and GABBR2 (GBR2) subunits.

Subtypes and Classification:

GABBRs are classified into two main subtypes: GABBR1 and GABBR2.

GABBR1 serves as the ligand-binding subunit, while GABBR2 is required for G protein coupling and signal transduction.

Physiological Functions:

• Inhibition of Neurotransmitter Release: Activation of GABBRs inhibits the release of neurotransmitters such as glutamate, leading to neuronal inhibition and reduced excitability.
• Synaptic Plasticity: GABBRs play roles in synaptic plasticity processes such as long-term potentiation (LTP) and long-term depression (LTD), which are fundamental for learning and memory.
• Regulation of Neuronal Excitability: GABBR activation hyperpolarizes neurons, decreasing their excitability and preventing excessive neuronal firing.

Clinical Implications:

• Neurological Disorders: Dysregulation of GABBR signaling has been implicated in various neurological disorders, including epilepsy, anxiety disorders, depression, schizophrenia, and neuropathic pain.
• Epilepsy: GABBR agonists have been investigated as potential antiepileptic drugs, while GABBR antagonists may exacerbate seizure activity.
• Psychiatric Disorders: GABBRs are potential targets for the development of novel treatments for anxiety, depression, and schizophrenia.