Dakshinamurti K, LeBlancq W D, Herchl R, Havlicek V
Exp Brain Res. 1976 Nov 23;26(4):355-66. doi: 10.1007/BF00234219.
The effects of a large number of neurotropic drugs have been attributed to changes in the metabolism of 5-hydroxytryptamine. The aromatic amino acid decarboxylase considered to decarboxylate both dihydroxyphenylalanine and 5-hydroxytryptophan requires pyridoxal phosphate as coenzyme. Thus, in pyridoxine deficiency one would expect a decrease of serotonin as well as the catecholamines of the brain. In the present study we have found a very significant decrease in brain serotonin of the pyridoxine-deficient growing rat. However, the brain levels of norepinephrine and dopamine were not altered. This decrease in serotonin does not result from a decrease either in the brain level of trytophan or the activity of tryptophan hydroxylase. Increased degradation of serotonin measured by the levels of its metabolite, 5-hydroxyindoleacetic acid is also excluded, thus suggesting the possibility that the decarboxylation of 5-hydroxytryptophan is decreased in pyridoxine deficiency.
大量神经营养药物的作用被认为与5-羟色胺代谢的变化有关。芳香族氨基酸脱羧酶被认为可使二羟基苯丙氨酸和5-羟色氨酸脱羧，它需要磷酸吡哆醛作为辅酶。因此，在吡哆醇缺乏的情况下，人们预期大脑中的血清素以及儿茶酚胺会减少。在本研究中，我们发现吡哆醇缺乏的生长中大鼠大脑中的血清素显著减少。然而，去甲肾上腺素和多巴胺的脑内水平未发生改变。血清素的这种减少并非由色氨酸的脑内水平降低或色氨酸羟化酶的活性降低所致。通过其代谢产物5-羟吲哚乙酸的水平测定，也排除了血清素降解增加的情况，因此提示在吡哆醇缺乏时5-羟色氨酸的脱羧作用可能降低。
