Drugs & Medication

Gamma-aminobutyric acid (usually abbreviated to GABA) is an inhibitory neurotransmitter found in the nervous systems of widely divergent species. It is the chief inhibitory neurotransmitter in the vertebrate central nervous system.

Gamma-aminobutyric acid
General
Systematic name	4-aminobutanoic acid
Other names	GABA
Molecular formula	C4H9NO2
SMILES	C(CC(=O)O)CN
Molar mass	103.12 g/mol
Appearance	white solid
CAS number	56-12-2
Properties
Solubility in water	? g/100 ml (? °C) or 0.5 M (20 °C)
Melting point	203°C (476 K)
Acidity (pKa)	10.43
Basicity (pKb)	9.77
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)

Contents 1 Action and receptors 2 Synthesis 3 Pharmacology 4 External links

Action and receptors

In vertebrates, GABA acts at inhibitory synapses in the brain. GABA acts by binding to specific receptors in the plasma membrane of both pre- and postsynaptic neurons. This binding causes the opening of ion channels to allow either the flow of negatively-charged chloride ions into the cell or positively-charged potassium ions out of the cell. This will typically result in a negative change in the transmembrane potential, usually causing hyperpolarization.

Three general classes of GABA receptor are known. These include GABA_A and GABA_C ionotropic receptors, which are ion channels themselves, and GABAB metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries (G proteins).

Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the vertebrate. Medium Spiny Cells are a typical example of inhibitory CNS GABAergic cells. GABA exhibits excitatory actions in insects, mediating muscle activation at synapses between nerves and muscle cells and also the stimulation of certain glands. GABA has also been shown to have excitatory roles in the vertebrate, most notably in the developing cortex.

Synthesis

Organisms synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor. It is worth noting that this involves converting the principal excitatory neurotransmitter (glutamate) into the principal inhibitory one (GABA).

Pharmacology

Drugs that act as agonists of GABA receptors (known as GABA analogues or GABAergic drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects. Many of the substances below are known to cause short-term memory loss and retrograde amnesia.

Drugs that affect GABA receptors:

• avermectins — doramectin, selamectin, ivermectin
• barbiturates
• bicucullines
• benzodiazepines
• baclofen
• tramadol
• opiates
• cannabinoids
• carbamazepines
  cyclopyrrolone derivatives — eszopiclone, zopiclone
  ethanol [1] [2]
• fluoroquinolones
• gabazine (SR-95531)
  gamma-hydroxybutyrate (GHB) [3]
• imidazopyridines — zaleplon, zolpidem
• muscimol
  phenytoin
  picrotoxin
  progabide
  propofol
  phenibut
  thujone
  valproate

Drugs that affect GABA in other ways:

• tiagabine - potentiates by inhibiting uptake into neurons and glia
• vigabatrin - potentiates by inhibiting GABA-T, preventing GABA breakdown

External links

• The role of GABA in the pathogenesis and treatment of anxiety and other neuropsychiatric disorders
• Link page to external chemical sources.