GABAerg

GABAerg, or GABAergic, refers to neurons, synapses, or signaling pathways that use gamma-aminobutyric acid (GABA) as their primary inhibitory neurotransmitter in the central nervous system. GABA is synthesized from glutamate by the enzyme glutamic acid decarboxylase (GAD) and released from presynaptic terminals to activate postsynaptic receptors.

GABA receptors are of several types. GABA-A receptors are ionotropic chloride channels that produce fast inhibitory postsynaptic potentials. GABA-B receptors are metabotropic, G-protein-coupled receptors that generate slower, longer-lasting inhibition via second messenger systems and ion channel modulation. A class previously called GABA-C is now generally considered a subtype of GABA-A receptors (GABA-A rho). Inhibitory signaling mediated by these receptors reduces neuronal excitability and helps regulate network activity.

In development, GABA signaling can be excitatory in immature neurons due to higher intracellular chloride levels; it typically becomes inhibitory as chloride homeostasis matures, aided by transporters such as NKCC1 and KCC2. Pharmacologically, GABAerg transmission can be modulated by drugs that enhance GABAergic signaling. Benzodiazepines and barbiturates enhance GABA-A function, baclofen is a GABA-B agonist, and inhibitors of GABA metabolism or reuptake (such as vigabatrin or tiagabine) increase synaptic GABA. These agents are used in anesthesia, epilepsy management, spasticity, and anxiety disorders.

GABAergic interneurons are widely distributed in the brain, notably in the cortex, hippocampus, and cerebellum, where they provide fast inhibitory control that shapes timing, oscillations, and information processing within neural circuits.