Vitamin serotonin formation

There is a great deal of evidence that deficiency of serotonin (5-hydroxytryptamine) is a factor in depressive illness, and many antidepressant drugs act to decrease its catabolism or enhance its interaction with receptors. A key enzyme involved in the synthesis of serotonin (and the catecholamines) is aromatic amino acid decarboxylase, which is pyridoxal phosphate-dependent. Therefore, it has been suggested that vitamin Be deficiency may result in reduced formation of the neurotransmitters and thus be a factor in the etiology of depression. Conversely, it has been suggested that supplements of vitamin Be may increase aromatic amino acid decarboxylase activity, and increase amine synthesis and have a mood-elevating or antidepressant effect. There is little evidence that vitamin Be deficiency affects the activity of aromatic amino acid decarboxylase. In patients with kidney failure, undergoing renal dialysis, the brain concentration of pyridoxal phosphate falls to about 50% of normal, with no effect on serotonin, catecholamines, or their metabolites (Perry etal., 1985). 

Central effects on blood pressure regulation as a result of decreased synthesis of brain GABA and serotonin (5-hydroxytryptamine). Glutamate decarboxylase activity in the nervous system is especially sensitive to vitamin Bg depletion, possibly as a result of mechanism-dependent inactivation by transamination. Although there is no evidence that aromatic amino acid decarboxylase activity is reduced in vitamin Bg deficiency, there is reduced formation of serotonin in the central nervous system. 

The enzyme L-aromatic amino acid decarboxylase (AADC, EC 4.1.1.28) lacks substrate specificity and has been considered to be involved in the formation of the catecholamines and serotonin. There are many differences in the optimal conditions for enzyme activity, including kinetics, affinity for PLP, activation and inhibition by specific chemicals, and regional differences in the distribution of DOPA and 5-HTP decarboxylation activities. Nonparallel changes in brain monoamines in the vitamin Bg-deficient rat have been reported (7-9). Brain content of dopamine and norepinephrine were not decreased during deficiency, whereas serotonin was significantly decreased. 

Also, vitamin C is required for the conversion of tryptophan to 5-hydroxytryptophan, the first step in the formation of the serotonin, a compound that raises blood pressure through vasoconstrictor action. 

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