GABA-A receptor

The GABA-A receptor is a ligand-gated ion channel activated by gamma-aminobutyric acid. It usually allows chloride ions to cross neuronal membranes, producing rapid inhibition.

Gamma-aminobutyric acid: Gamma-aminobutyric acid is the principal inhibitory neurotransmitter in the mature mammalian brain. Binding of this neurotransmitter opens the receptor’s ion channel.
Benzodiazepine: Benzodiazepines are drugs that enhance GABA-A receptor responses at specific allosteric binding sites. They increase the effect of GABA without directly opening the channel.
Allosteric modulation: Allosteric modulation occurs when a molecule changes a protein’s activity by binding away from its primary functional site. Many drugs change channel responses through sites separate from GABA’s binding site.
GABAergic signaling: GABAergic signaling is communication mediated by gamma-aminobutyric acid and its receptors. This receptor is a major source of GABA’s fast inhibitory effects.
Extrasynaptic GABA-A receptor: An extrasynaptic GABA-A receptor is located outside synaptic specializations and often responds to ambient GABA. These receptors sustain tonic currents that differ from brief synaptic responses.
Chloride channel: A chloride channel is a membrane protein that permits chloride ions to cross a cell membrane. The GABA-A receptor is a ligand-gated member of this channel family.
Barbiturate: Barbiturates are central nervous system depressants that enhance GABA-A receptor function at high concentrations. Their receptor modulation contributes to sedation, anesthesia, and seizure control.
Ionotropic receptor: An ionotropic receptor is a membrane receptor that directly controls an ion channel when a ligand binds. GABA-A receptors are ionotropic, unlike slower G-protein-coupled GABA receptors.
Epilepsy: Epilepsy is a neurological disorder characterized by a lasting tendency to produce unprovoked seizures. Impaired inhibitory signaling can contribute to seizure generation and is a treatment target.
Tonic inhibition: Tonic inhibition is persistent suppression of neuronal excitability produced by ongoing extrasynaptic receptor activity. It reveals receptor effects that cannot be explained by synaptic currents alone.

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