Gamma-aminobutyric acid (GABA)  can account for approximately 40% of the inhibitory processing in the brain --> main inhibitory transmitter in the brain of mammalians.
GABA occurs in brain tissue but not in other tissues, except in trace amounts. However GABA has pharmacological functions also outside of CNS.

Neurotransmission occurs via the vesicular release of neurotransmitters at presynaptic nerve terminals. Specifically, calcium-evoked exocytosis of the presynaptic vesicles is what enables the release of neurotransmitters into the SYNAPTIC CLEFT. 

GABA is formed from glutamate by the action of glutamic acid decarboxylase (GAD), an enzyme found only in GABA-synthesising neurons in the brain.

GABAergic neurons and astrocytes take up GABA via specific transporters (++ GAT1) thus removing GABA after it has been released and reciclying it. 

About 20% of CNS neurons are GABAergic; most are short interneurons, but there are some long GABAergic tracts, e.g. from the striatum to the substantia nigra and globus pallidus.

GABA acts on two distinct types of receptor: GABAA receptors are ligand-gated ion channels whereas GABAB receptors are G protein–coupled. (GABAC now included in GABAA family unclear pharmacological role)

GABAA: heteropentameric,- ionotropic of Cis-loop family each receptor contains two α, two β and one γ subunit arranged in a circle in the sequence α–β–α–β–γ around the pore when viewed from the extracellular side of the membrane.
19 receptors subunit: (α1–6, β1–3, γ1–3, δ, ε, θ, π and ρ1–3). The receptor composition and arrangement influence its functional and pharmacological properties.
The most common (more studied) is α1β2γ2.
located postsynaptically and mediate both fast and tonic inhibition. The GABAA channel is selectively permeable to Cl⁻ and because the equilibrium membrane potential for Cl⁻ is usually negative to the resting potential, increasing Cl⁻ permeability hyperpolarises the cell as Cl⁻ ions enter, thereby reducing its excitability.
In the postsynaptic cell, GABAA receptors are located both intrasynaptically and extrasynaptically.
Thus, GABA produces inhibition by acting both as a fast ‘point-to-point’ transmitter and as an ‘action-at-a-distance’ neuromodulator, as the extrasynaptic GABAA receptors can be tonically activated by GABA that has diffused away from its site of release. Extrasynaptic GABAA have higher affinity for GABA and show less desensitisation than intrasynaptic receptors, and are also highly sensitive to general anaesthetic agents and ethanol.

GABAB receptors are G-protein-coupled receptors (GPCRs) for GABA located presynaptically and postsynaptically. They activate separate cation channel through 
glicoprotein --> inhibition of voltage-gated Ca2+ channels (thus reducing transmitter release), opening of potassium channels ( potassium ions go out! thus reducing postsynaptic excitability) and to inhibit adenylyl cyclase. 

GABAC now called GABAA-ρ receptors (subfamily GABAA) after UPHAR (international Unit of Basic and Clinical pharmacology) NOMENCLATURE COMMITTEE has recommended (2009) that due to structure similarities with GABAA: pentameric Cl⁻ -permeable ligand-gated channels comprising homo- or heteromeric assemblies of ρ subunits.

Neurosteroids are compounds that are related to steroid hormones but that act to enhance activation of GABAA receptors. Endogenous --> metabolite of progesterone and androgens. 
anaesthetics --> alfaxalone. 

Benzodiazepines bind with high affinity to an accessory allosteric site on the GABAA receptor (α-γ) lead to a conformational change in the receptor such as to increase the apparent affinity for channel gating by GABA at both agonist sites. As a result the GABA concentration channel opening curve is shifted to lower GABA concentrations (Fig. 4B). At the single channel level, benzodiazepines increase mean open times.
barbiturates, volatile agents, ethanol
propofol (β) may also activate the Cl^- channel alone at high concentrations 

ketamine is potentiating /modulating GABA A (subunit α6)

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Sarmazenil is an inverse agonist of benzodiazepine at GABAA
Flumazenil is a competetitive antagonist of benzodiazepine at GABAA