Gamma-aminobutyric acid
From Wikipedia, the free encyclopedia
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 | |
| Density and phase | ? g/cm3, ? |
| Solubility in water | ? g/100 ml (? °C) or 0.5 M (20 °C) |
| Melting point | 203°C (476 K) |
| Boiling point | ? °C (? K) |
| Acidity (pKa) | 10.43 |
| Basicity (pKb) | 9.77 |
| Chiral rotation [α]D | ?° |
| Viscosity | ? cP at ? °C |
| Structure | |
| Molecular shape | ? |
| Coordination geometry |
? |
| Crystal structure | ? |
| Dipole moment | ? D |
| Hazards | |
| MSDS | External MSDS |
| Main hazards | ? |
| NFPA 704 | |
| Flash point | ? °C |
| R/S statement | R: ? S: ? |
| RTECS number | ? |
| Supplementary data page | |
| Structure and properties |
n, εr, etc. |
| Thermodynamic data |
Phase behaviour Solid, liquid, gas |
| Spectral data | UV, IR, NMR, MS |
| Related compounds | |
| Other anions | ? |
| Other cations | ? |
| Related ? | ? |
| Related compounds | ? |
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) Infobox disclaimer and references |
|
Contents |
[edit] 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 GABAA and GABAC 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.
[edit] 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).
[edit] 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
