Autor: |
Oxenkrug GF; Department of Psychiatry, Tufts University, 750 Washington St., Ste. 1007, Boston, MA 02111, USA. goxenkrug@tufts-nemc.org, Sablin SO, Requintina PJ |
Jazyk: |
angličtina |
Zdroj: |
Annals of the New York Academy of Sciences [Ann N Y Acad Sci] 2007 Dec; Vol. 1122, pp. 245-52. |
DOI: |
10.1196/annals.1403.017 |
Abstrakt: |
The ability of methylene blue (MB) to inhibit the nitric oxide-induced stimulation of N-methyl-D-aspartate receptors has been suggested as a possible mechanism of MB's clinical antidepressant action. This study evaluated the alternative/additional mechanisms of the antidepressant effect of MB on biochemical and behavior levels. Selective inhibition of monoamine oxidase type A (MAO-A) is widely accepted as a major mechanism of the clinical antidepressant effect. MB and the related redox dyes toluidine blue O (TBO), thionine (TN), brilliant cresyl blue (BCB), and toluylene blue (TB) were reversible competitive inhibitors of both MAO-A and MAO-B and were highly selective toward MAO-A. TBO was the most potent inhibitor, followed by TN, BCB, MB, and TB. The dyes studied increased rat pineal N-acetylserotonin (NAS) and melatonin content, in accordance with our previous observations of the stimulating effect of selective inhibition of MAO-A on pineal melatonin biosynthesis. The redox dyes exerted antidepressant-like activity in frogs; that is, they suppressed the righting reflex in melatonin-primed frogs. This study's results indicate that selective inhibition of MAO-A might mediate the clinical antidepressant effect of MB through NAS stimulation and melatonin biosynthesis. |
Databáze: |
MEDLINE |
Externí odkaz: |
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