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In [[pharmacology]], a '''GABA transaminase inhibitor''' is an [[enzyme inhibitor]] that acts upon [[GABA transaminase]].<ref name="Ciesielski 1979">{{Cite journal
In [[pharmacology]], a '''GABA transaminase inhibitor''' is an [[enzyme inhibitor]] that acts upon [[GABA transaminase]].<ref name="Ciesielski 1979">{{Cite book
| doi = 10.1007/978-1-4899-5199-1_2
| doi = 10.1007/978-1-4899-5199-1_2
| last1 = Ciesielski | first1 = L.
| last1 = Ciesielski | first1 = L.
Line 10: Line 10:
| last8 = Cohen-Addad | first8 = C.
| last8 = Cohen-Addad | first8 = C.
| last9 = Lajzerowicz | first9 = J.
| last9 = Lajzerowicz | first9 = J.
| title = GABA—Biochemistry and CNS Functions | chapter = GABA Transaminase Inhibitors | series = Advances in Experimental Medicine and Biology | volume = 123
| title = GABA transaminase inhibitors
| journal = Advances in Experimental Medicine and Biology
| volume = 123
| pages = 21–41
| pages = 21–41
| year = 1979
| year = 1979
Line 45: Line 43:
| year = 1990
| year = 1990
| pmid = 2399411 | doi=10.1177/019262339001800201
| pmid = 2399411 | doi=10.1177/019262339001800201
| doi-access = free
}}</ref> [[phenylethylidenehydrazine]] (and drugs that metabolize to it, such as [[phenelzine]]<ref>{{Cite journal|last=McKenna|first=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}}</ref>), [[Ethanolamine-O-sulfate|ethanolamine-''O''-sulfate]] (EOS), and L-[[cycloserine]].<ref name="Polc 1986">{{Cite journal
}}</ref> [[phenylethylidenehydrazine]] (and drugs that metabolize to it, such as [[phenelzine]]<ref>{{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 }}</ref>), [[Ethanolamine-O-sulfate|ethanolamine-''O''-sulfate]] (EOS), and L-[[cycloserine]].<ref name="Polc 1986">{{Cite journal
| doi = 10.1016/0028-3908(86)90236-4
| doi = 10.1016/0028-3908(86)90236-4
| last1 = Polc | first1 = P.
| last1 = Polc | first1 = P.
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| year = 1986
| year = 1986
| pmid = 3012401
| pmid = 3012401
}}</ref>
| s2cid = 462885 }}</ref>


Certain members of this class are used as [[anticonvulsant]]s.
Certain members of this class are used as [[anticonvulsant]]s.

Latest revision as of 21:12, 2 September 2023

In pharmacology, a GABA transaminase inhibitor is an enzyme inhibitor that acts upon GABA transaminase.[1] Inhibition of GABA transaminase enzymes reduces the degradation of GABA, leading to increased neuronal GABA concentrations.

Examples include valproic acid,[2] vigabatrin,[3][4] phenylethylidenehydrazine (and drugs that metabolize to it, such as phenelzine[5]), ethanolamine-O-sulfate (EOS), and L-cycloserine.[6]

Certain members of this class are used as anticonvulsants.

References

[edit]
  1. ^ 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. ISBN 978-1-4899-5201-1. PMID 390993.
  2. ^ 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.
  3. ^ 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.
  4. ^ 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.
  5. ^ 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". Journal of Neural Transmission. Supplementum. 41: 115–122. doi:10.1007/978-3-7091-9324-2_15. ISBN 978-3-211-82521-1. ISSN 0303-6995. PMID 7931216.
  6. ^ 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.
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