Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tryptophan uptake, hydroxylation, and decarboxylation in isolated synaptosomes were studied to assess how their properties may determine the rate of serotonin synthesis in the presynaptic nerve terminals of the brain. Simultaneous measurements of the rates of uptake, hydroxylation, and decarboxylation in the presence and absence of various inhibitors showed that tryptophan hydroxylase is rate-limiting for serotonin synthesis in this model system. There was significant direct decarboxylation of tryptophan to tryptamine. Measurement of tryptophan hydroxylase flux with varying internal concentrations of tryptophan allowed the determination of the Km of tryptophan hydroxylase in synaptosomes for tryptophan of 120 +/- 15 microM. Depolarisation of synaptosomes with veratridine caused both a reduction in the internal tryptophan concentration and an apparent activation of tryptophan hydroxylase. This activation did not occur in the absence of Ca2+ or in the presence of trifluoperazine. Synaptosomal serotonin synthesis and brain stem-soluble tryptophan hydroxylase were inhibited by low concentrations of noradrenaline or dopamine. Dibutyryl cyclic AMP, glucagon, insulin, and vasopressin were observed to have no effect on tryptophan uptake or hydroxylation in synaptosomes.
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PMID:Tryptophan uptake and hydroxylation in rat forebrain synaptosomes. 669 97

The effects of water deprivation and hydration on plasma corticosterone concentration and the activity of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin (5-HT) biosynthesis, in the hypothalamus of vasopressin- (AVP-) deficient homozygous Brattleboro and normal Wistar rats were studied. In the Wistar rats, water deprivation caused an increase in the TPH activity in the anterior and middle (infundibular) parts of the hypothalamus, while hydration did not affect the activity of the enzyme in the anterior hypothalamus but produced an increase in its middle part. In contrast, in the Brattleboro rats, water deprivation had no effect on TPH activity in the anterior and middle parts of the hypothalamus but hydration produced a decrease in TPH activity in the anterior hypothalamus. After 48 h of water deprivation, the plasma corticosterone concentration significantly increased in water-deprived and decreased in hydrated Wistar rats. Under water deprivation, the rise in corticosterone concentration in the homozygous Brattleboro rats was significantly greater than that in the Wistar rats. The data provide evidence that the CRH-like activity of AVP is not necessary for activation of the hypothalamic-pituitary-adrenal system induced by water deprivation. The observations show that AVP is involved in the activation of TPH induced by water deprivation. This suggests that AVP modulates the metabolism of 5-HT and the response of the 5-HT-ergic system to water deprivation.
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PMID:Hypothalamic tryptophan hydroxylase and the hypothalamic-pituitary-adrenocortical response to water deprivation and hydration in vasopressin-deficient and normal rats. 1211 Dec 45