GABA transaminase inhibitor: Difference between revisions
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In [[pharmacology]], a '''GABA transaminase inhibitor''' is an [[enzyme inhibitor]] that acts upon [[GABA transaminase]].<ref name="Ciesielski 1979">{{Cite book |
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| doi = 10.1007/978-1-4899-5199-1_2 |
| doi = 10.1007/978-1-4899-5199-1_2 |
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| last1 = Ciesielski | first1 = L. |
| last1 = Ciesielski | first1 = L. |
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| Line 10: | Line 10: | ||
| last8 = Cohen-Addad | first8 = C. |
| last8 = Cohen-Addad | first8 = C. |
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| last9 = Lajzerowicz | first9 = J. |
| last9 = Lajzerowicz | first9 = J. |
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| title = GABA—Biochemistry and CNS Functions | chapter = GABA Transaminase Inhibitors | series = Advances in Experimental Medicine and Biology | volume = 123 |
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| title = GABA transaminase inhibitors |
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| series = Advances in Experimental Medicine and Biology |
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| journal = Advances in Experimental Medicine and Biology |
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| volume = 123 |
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| pages = 21–41 |
| pages = 21–41 |
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| year = 1979 |
| year = 1979 |
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| Line 19: | Line 16: | ||
| pmid = 390993 |
| pmid = 390993 |
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}}</ref> |
}}</ref> |
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Inhibition of GABA transaminase enzymes reduces the degradation of GABA, leading to increased neuronal GABA concentrations. |
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Examples include [[valproic acid]],<ref>{{Cite journal |
Examples include [[valproic acid]],<ref>{{Cite journal |
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| Line 31: | Line 29: | ||
| year = 1979 |
| year = 1979 |
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| pmid = 110294 |
| pmid = 110294 |
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}}</ref> [[vigabatrin]],<ref name="pmid18412635">{{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 |
}}</ref> [[vigabatrin]],<ref name="pmid18412635">{{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}}</ref><ref>{{Cite journal |
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| last1 = Gibson | first1 = J. P. |
| last1 = Gibson | first1 = J. P. |
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| last2 = Yarrington | first2 = J. T. |
| last2 = Yarrington | first2 = J. T. |
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| last6 = Newberne | first6 = J. W. |
| last6 = Newberne | first6 = J. W. |
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| title = Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor |
| title = Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor |
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| journal = Toxicologic |
| journal = Toxicologic Pathology |
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| volume = 18 |
| volume = 18 |
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| issue = 2 |
| issue = 2 |
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| Line 45: | Line 43: | ||
| year = 1990 |
| year = 1990 |
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| pmid = 2399411 | doi=10.1177/019262339001800201 |
| pmid = 2399411 | doi=10.1177/019262339001800201 |
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| doi-access = free |
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}}</ref> [[phenylethylidenehydrazine]], [[Ethanolamine-O-sulfate|ethanolamine-''O''-sulfate]] (EOS), and L-[[cycloserine]].<ref name="Polc 1986">{{Cite journal |
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}}</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 |
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| doi = 10.1016/0028-3908(86)90236-4 |
| doi = 10.1016/0028-3908(86)90236-4 |
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| last1 = Polc | first1 = P. |
| last1 = Polc | first1 = P. |
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| Line 62: | Line 61: | ||
| year = 1986 |
| year = 1986 |
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| pmid = 3012401 |
| pmid = 3012401 |
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}}</ref> |
| s2cid = 462885 }}</ref> |
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Certain members of this class are used as [[anticonvulsant]]s. |
Certain members of this class are used as [[anticonvulsant]]s. |
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There is some evidence that ''[[Melissa officinalis]]'' (lemon balm), and the [[rosmarinic acid]] it contains, inhibits GABA transaminase.<ref>{{Cite journal |
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| last1 = Awad | first1 = R. |
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| last2 = Levac | first2 = D. |
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| last3 = Cybulska | first3 = P. |
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| last4 = Merali | first4 = Z. |
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| last5 = Trudeau | first5 = V. L. |
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| last6 = Arnason | first6 = J. T. |
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| doi = 10.1139/Y07-083 |
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| title = Effects of traditionally used anxiolytic botanicals on enzymes of the γ -aminobutyric acid (GABA) systemThis article is one of a selection of papers published in this special issue (part 1 of 2) on the Safety and Efficacy of Natural Health Products |
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| journal = Canadian Journal of Physiology and Pharmacology |
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| volume = 85 |
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| issue = 9 |
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| pages = 933–942 |
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| year = 2007 |
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| pmid = 18066140 |
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| pmc = |
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}}</ref> |
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== References == |
== References == |
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{{Enzyme inhibition}} |
{{Enzyme inhibition}} |
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[[Category:GABA transaminase inhibitors| |
[[Category:GABA transaminase inhibitors| ]] |
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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]- ^ 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.
- ^ 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". 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.
- ^ 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.