Instability in the response to DST in major depressions during treatment with 5-hydroxytryptophan and carbidopa.
During the course of an investigation of predictors of the therapeutic response to a precursor of serotonin (5-hydroxytryptophan, 5-HTp) associated with carbidopa in major depressions with melancholia, patients, who before the treatment behaved as suppressors in the DST, became non-suppressors. The variation from non-suppressor to suppressor (which yielded in 60% of this sample) can be explained by the clinical improvement, but not the inverse change. In this paper, different possibilities on this change are analyzed, the most probable being the direct effect of the carbidopa in eminentia media. The carbidopa is administered because it is an inhibitor of the aminoacid decarboxylase, and since it does not cross the hematoencephalic barrier, it permits a better use of the 5-HTp. However, there is an exception: it does act in the cells of the eminentia media which, from the functional point of view, lie outside the above-mentioned hematoencephalic barrier.
D006916:5-Hydroxytryptophan / Q000008:administration & dosage*; D000293:Adolescent; D000328:Adult; D000368:Aged; D001714:Bipolar Disorder / Q000188:drug therapy* / Q000503:physiopathology; D002230:Carbidopa / Q000008:administration & dosage*; D003866:Depressive Disorder / Q000188:drug therapy* / Q000503:physiopathology; D003907:Dexamethasone; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000503:physiopathology
D003907:Dexamethasone; D006916:5-Hydroxytryptophan; D002230:Carbidopa; D006854:Hydrocortisone