GABA transaminase inhibitor
In pharmacology, a GABA transaminase inhibitor is an enzyme inhibitor that acts upon GABA transaminase.{{Cite book
| doi = 10.1007/978-1-4899-5199-1_2
| last1 = Ciesielski | first1 = L.
| last2 = Simler | first2 = S.
| last3 = Gensburger | first3 = C.
| last4 = Mandel | first4 = P.
| last5 = Taillandier | first5 = G.
| last6 = Benoit-Guyod | first6 = J. L.
| last7 = Boucherle | first7 = A.
| last8 = Cohen-Addad | first8 = C.
| last9 = Lajzerowicz | first9 = J.
| title = GABA—Biochemistry and CNS Functions | chapter = GABA Transaminase Inhibitors | series = Advances in Experimental Medicine and Biology | volume = 123
| pages = 21–41
| year = 1979
| isbn = 978-1-4899-5201-1
| pmid = 390993
}}
Inhibition of GABA transaminase enzymes reduces the degradation of GABA, leading to increased neuronal GABA concentrations.
Examples include valproic acid,{{Cite journal
| doi = 10.1001/archneur.1979.00500430023002
| last1 = Bruni | first1 = J.
| last2 = Wilder | first2 = B. J.
| title = Valproic acid. Review of a new antiepileptic drug
| journal = Archives of Neurology
| volume = 36
| issue = 7
| pages = 393–398
| year = 1979
| pmid = 110294
}} vigabatrin,{{cite journal |vauthors=Wang QP, Jammoul F, Duboc A |title=Treatment of epilepsy: the GABA-transaminase inhibitor, vigabatrin, induces neuronal plasticity in the mouse retina |journal=Eur. J. Neurosci. |volume=27 |issue=8 |pages=2177–87 |date=April 2008 |pmid=18412635 |pmc=2933832 |doi=10.1111/j.1460-9568.2008.06175.x |display-authors=etal}}{{Cite journal
| last1 = Gibson | first1 = J. P.
| last2 = Yarrington | first2 = J. T.
| last3 = Loudy | first3 = D. E.
| last4 = Gerbig | first4 = C. G.
| last5 = Hurst | first5 = G. H.
| last6 = Newberne | first6 = J. W.
| title = Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor
| journal = Toxicologic Pathology
| volume = 18
| issue = 2
| pages = 225–238
| year = 1990
| pmid = 2399411 | doi=10.1177/019262339001800201
| doi-access = free
}} phenylethylidenehydrazine (and drugs that metabolize to it, such as phenelzine{{Cite journal|last1=McKenna|first1=K. F.|last2=McManus|first2=D. J.|last3=Baker|first3=G. B.|last4=Coutts|first4=R. T.|date=1994|title=Chronic administration of the antidepressant phenelzine and its N-acetyl analogue: effects on GABAergic function|url=https://pubmed.ncbi.nlm.nih.gov/7931216/|journal=Journal of Neural Transmission. Supplementum|volume=41|pages=115–122|doi=10.1007/978-3-7091-9324-2_15|issn=0303-6995|pmid=7931216|isbn=978-3-211-82521-1 }}), ethanolamine-O-sulfate (EOS), and L-cycloserine.{{Cite journal
| doi = 10.1016/0028-3908(86)90236-4
| last1 = Polc | first1 = P.
| last2 = Pieri | first2 = L.
| last3 = Bonetti | first3 = E. P.
| last4 = Scherschlicht | first4 = R.
| last5 = Moehler | first5 = H.
| last6 = Kettler | first6 = R.
| last7 = Burkard | first7 = W.
| last8 = Haefely | first8 = W.
| title = L-cycloserine: Behavioural and biochemical effects after single and repeated administration to mice, rats and cats
| journal = Neuropharmacology
| volume = 25
| issue = 4
| pages = 411–418
| year = 1986
| pmid = 3012401
| s2cid = 462885 }}
Certain members of this class are used as anticonvulsants.