GABAergic

GABAergic refers to anything that uses gamma-aminobutyric acid (GABA) as its neurotransmitter, receptor, or mechanism of action. GABA is the principal inhibitory neurotransmitter of the mammalian central nervous system, synthesized from glutamate by the enzyme glutamate decarboxylase (GAD65/67) and loaded into synaptic vesicles by the vesicular GABA transporter (VGAT). GABAergic neurons are widespread and often function as interneurons that modulate excitatory circuits and network activity.

GABA signals through three receptor families: GABA_A, GABA_B, and GABA_C (also called GABA_A-ρ). GABA_A and GABA_C are ion channels that permit chloride influx, producing fast inhibition. GABA_B receptors are metabotropic and cause slower, longer-lasting inhibition by opening potassium channels and suppressing calcium influx.

In development, GABA can be depolarizing due to chloride gradients but becomes inhibitory in mature neurons. GABAergic signaling shapes excitability, synchronizes oscillations, and maintains the balance between excitation and inhibition in neural circuits.

Dysfunction or altered GABAergic signaling is linked to epilepsy, anxiety, sleep disorders, and other neurological conditions. Clinically, drugs that enhance GABAergic transmission—such as GABA_A receptor positive allosteric modulators (benzodiazepines, barbiturates), GABA_B agonists (baclofen), or agents that raise GABA levels (vigabatrin, tiagabine)—are used to modulate inhibitory signaling.