Gamma-aminobutyric acid (GABA) is a neurotransmitter in widely divergent species. In humans, GABA acts at inhibitory synapses in the brain and spinal cord. As in the other contexts where GABA acts as a transmitter, the inhibition results from a hyperpolarization of the synaptic transmembrane potential of the inhibited neuron, which is elicited by the binding of GABA molecules to specific receptors in the plasma membrane of both pre- and post-synaptic cells. This binding opens ion channels to allow either the flow of chloride or potassium ions into or out of the cell. In insects GABA mediates muscle activation at synapses between nerves and muscle cells and also the stimulation of certain glands. So far three general classes of GABA receptor are known, more than one of which is often represented in the same organisms. These include both so-called ionotropic receptors, which are ion channels themselves, and metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries (G proteins).

With regard to the human brain, it has been asserted that GABA signals interfere with the registration and consolidation stages of memory formation. This is thought to be possible because the GABA system is found in the hippocampus, an area of brain which has been implicated in memory formation.

Organisms synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor.

Three types of GABA receptors:

• GABA_A receptors
• GABA_B receptors
• GABA_C receptors

Drugs which affect GABA receptors:

• alcohol
• bicuculline
• benzodiazepines and barbiturates
• baclofen
• carbamazepine, phenytoin, valproate
• gamma-hydroxybutyrate (GHB)
• picrotoxin
• propofol
• thujone
• zolpidem, zopiclone

External links

• http://www.vcu-cme.org/gaba/overview2.html