Gamma-aminobutyric acid

From Citizendium, the Citizens' Compendium

Gamma aminobutyric acid (GABA) or -aminobutyrate, is the major inhibitory neurotransmitter in the central nervous system.^[1] GABA is produced from the amino acid glutamate through the action of the enzyme glutamate decarboxylase, and is inactivated by degradation to succinate in a two step mechanism involving the enzymes GABA-glutamate transaminase and succinate semialdehyde dehydrogenase.

Contents 1 Role in clinical pharmacology 1.1 Gamma-aminobutyric acid (GABA) agonists 1.1.1 Barbituates 1.1.2 Benzodiazepines 1.1.2.1 Non-selective agonists 1.1.2.2 BZ1 selective agonists 2 References

Role in clinical pharmacology

Gamma-aminobutyric acid (GABA) agonists

Drugs that increase the effect of GABA are called GABAergic.

Many sedatives work by increasing receptiveness of GABA_A receptors.

Barbituates

Barbituates are GABAergic by increasing receptiveness of the GABA_A receptors. Barbituates do this by increasing the duration of openings of channels in the cell membrane.^[1]

• Phenobarbital

Benzodiazepines

Benzodiazepines are also GABAergic by increasing receptiveness of the GABA_A receptors. However, benzodiazepines do this by increasing the frequency of openings of channels in the cell membrane.^[1]

Benzodiazepine receptors are BZ₁ and BZ₂.

Non-selective agonists

• Diazepam (Valium)

BZ₁ selective agonists

Cyclopyrrolones / Piperazines

• Zopiclone
• Eszopiclone

Imidazopyridines

• Zolpidem (Ambien)

Pyrazolopyrimidines

• Zaleplon (Sonata; Starnoc). May have similar abuse potential to benzodiazepams.^[2]

References

1. ↑ ^{1.0 1.1 1.2} Katzung, Bertram G. (2006). Basic and clinical pharmacology. New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-145153-6. 
2. ↑ Rush CR, Frey JM, Griffiths RR (1999). Zaleplon and triazolam in humans: acute behavioral effects and abuse potential.. Psychopharmacology (Berl) 145 (1): 39-51. PMID 10445371.