GABA transaminase inhibitor
| GABA transaminase inhibitor | |
|---|---|
| Drug class | |
 Vigabatrin (Sabril; γ-vinyl-GABA), a selective and irreversible GABA-T inhibitor used as an anticonvulsant.[1][2][3] | |
| Class identifiers | |
| Synonyms | GABA-T inhibitor; GABA metabolism inhibitor; GABA degradation inhibitor |
| Use | Epilepsy |
| Mechanism of action | GABA transaminase inhibition |
| Biological target | GABA transaminase (GABA-T) |
| Chemical class | GABA analogues and others |
| Legal status | |
| In Wikidata | |
A GABA transaminase inhibitor is a drug that acts as an inhibitor of the enzyme GABA transaminase (GABA-T), which metabolizes the major inhibitory neurotransmitter γ-aminobutyric acid (GABA).[2][4] Inhibition of GABA-T reduces the degradation of GABA, leading to increased neuronal GABA concentrations.[2] Examples of GABA-T inhibitors include valproic acid,[5] vigabatrin,[6][7] phenylethylidenehydrazine (PEH) (a metabolite of phenelzine),[8] ethanolamine-O-sulfate (EOS), and L-cycloserine, among others.[9] Certain GABA-T inhibitors, like vigabatrin, are used clinically as anticonvulsants.[2][3]
See also
[edit]- GABA reuptake inhibitor
- GABA receptor agonist
- GABAA receptor agonist
- GABAA receptor positive allosteric modulator
References
[edit]- ^ Connelly JF (February 1993). "Vigabatrin". Ann Pharmacother. 27 (2): 197–204. doi:10.1177/106002809302700215. PMID 8439699.
- ^ a b c d Sarup A, Larsson OM, Schousboe A (August 2003). "GABA transporters and GABA-transaminase as drug targets". Curr Drug Targets CNS Neurol Disord. 2 (4): 269–277. doi:10.2174/1568007033482788. PMID 12871037.
- ^ a b Angehagen M, Ben-Menachem E, Rönnbäck L, Hansson E (February 2003). "Novel mechanisms of action of three antiepileptic drugs, vigabatrin, tiagabine, and topiramate". Neurochem Res. 28 (2): 333–340. doi:10.1023/a:1022393604014. PMID 12608706.
- ^ Ciesielski, L.; Simler, S.; Gensburger, C.; Mandel, P.; Taillandier, G.; Benoit-Guyod, J. L.; Boucherle, A.; Cohen-Addad, C.; Lajzerowicz, J. (1979). "GABA Transaminase Inhibitors". GABA—Biochemistry and CNS Functions. Advances in Experimental Medicine and Biology. Vol. 123. pp. 21–41. doi:10.1007/978-1-4899-5199-1_2 (inactive 17 July 2025). ISBN 978-1-4899-5201-1. PMID 390993.
{{cite book}}: CS1 maint: DOI inactive as of July 2025 (link) - ^ Bruni, J.; Wilder, B. J. (1979). "Valproic acid. Review of a new antiepileptic drug". Archives of Neurology. 36 (7): 393–398. doi:10.1001/archneur.1979.00500430023002. PMID 110294.
- ^ Wang QP, Jammoul F, Duboc A, et al. (April 2008). "Treatment of epilepsy: the GABA-transaminase inhibitor, vigabatrin, induces neuronal plasticity in the mouse retina". Eur. J. Neurosci. 27 (8): 2177–87. doi:10.1111/j.1460-9568.2008.06175.x. PMC 2933832. PMID 18412635.
- ^ Gibson, J. P.; Yarrington, J. T.; Loudy, D. E.; Gerbig, C. G.; Hurst, G. H.; Newberne, J. W. (1990). "Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor". Toxicologic Pathology. 18 (2): 225–238. doi:10.1177/019262339001800201. PMID 2399411.
- ^ McKenna, K. F.; McManus, D. J.; Baker, G. B.; Coutts, R. T. (1994). "Chronic administration of the antidepressant phenelzine and its N-acetyl analogue: Effects on GABAergic function". Amine Oxidases: Function and Dysfunction. Vol. 41. pp. 115–122. doi:10.1007/978-3-7091-9324-2_15. ISBN 978-3-211-82521-1. ISSN 0303-6995. PMID 7931216.
- ^ Polc, P.; Pieri, L.; Bonetti, E. P.; Scherschlicht, R.; Moehler, H.; Kettler, R.; Burkard, W.; Haefely, W. (1986). "L-cycloserine: Behavioural and biochemical effects after single and repeated administration to mice, rats and cats". Neuropharmacology. 25 (4): 411–418. doi:10.1016/0028-3908(86)90236-4. PMID 3012401. S2CID 462885.