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Gamma-aminobutyric Acid





ACTION AND RECEPTORS

In Vertebrates , GABA acts at Inhibitory Synapse s in the Central Nervous System . GABA acts by binding to specific Receptor s in the Plasma Membrane of both pre- and postsynaptic cells. This binding causes the opening of Ion Channel s to allow either the flow of negatively-charged Chloride ions into or positively-charged Potassium ions out of the Cell . This will typically result in a negative change in the Transmembrane Potential .

In Insect s, GABA mediates Muscle activation at synapses between Nerve s and muscle cells and also the stimulation of certain Gland s.

Three general classes of GABA receptor are known. These include GABAA and GABAC Ionotropic Receptor s, which are ion channels themselves, and GABAB Metabotropic Receptor s, which are G Protein-coupled Receptor s that open ion channels via intermediaries ( G Protein s).


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 into the principal Inhibitory one.


PHARMACOLOGY

Drugs that act as Agonist s of GABA receptors (known as GABA analogues) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects.

Drugs that affect GABA receptors:

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

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