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5- Hydroxyindoleacetic acid

B.-M. Eriksson and B.-A. Persson, Determination of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in plasma by direct injection in coupled-column liquid clrromatography with electrochemical detection , 7. Chromatogr. 459 351-360 (1988). [Pg.295]

Figure 9.4 The synthesis and metabolism of 5-HT. The primary substrate for the pathway is the essential amino acid, tryptophan and its hydroxylation to 5-hydrox5dryptophan is the rate-limiting step in the synthesis of 5-HT. The cytoplasmic enzyme, monoamine oxidase (MAOa), is ultimately responsible for the catabolism of 5-HT to 5-hydroxyindoleacetic acid... Figure 9.4 The synthesis and metabolism of 5-HT. The primary substrate for the pathway is the essential amino acid, tryptophan and its hydroxylation to 5-hydrox5dryptophan is the rate-limiting step in the synthesis of 5-HT. The cytoplasmic enzyme, monoamine oxidase (MAOa), is ultimately responsible for the catabolism of 5-HT to 5-hydroxyindoleacetic acid...
HT is metabolised primarily by MAO to 5-hydroxyindoleacetic acid (5-HIAA) (Fig. 9.4). In vitro, 5-HT is the preferred substrate for the MAOa, rather than the MAOb isoenzyme (see Chapter 8) and this appears to be the case in vivo since MAOa, but not MAOb, knock-out mice have increased concentrations of 5-HT in the brain. Obviously, because of its indole nucleus, 5-HT is not a substrate for the enzyme COMT which metabolises the catechol derivatives, dopamine and noradrenaline. However, other metabolic products of 5-HT are theoretically possible and one, 5-hydroxytryptophol,... [Pg.196]

When administered in doses higher than 12 mg/kg/day, depletions of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) last up to 6 months after cessation of drug treatment (Harvey and McMaster 1975 Harvey et al. 1977 Clineschmidt et al. 1978 Steranka and Sanders-Bush 1979 Schuster et al. 1986 Kleven et al. 1988). Other long-lasting effects of fenfluramine include a decrease in 5-HT uptake sites (Schuster et al. 1986) and tryptophan hydroxylase activity (Steranka and Sanders-Bush 1979). [Pg.149]

This chapter will review some recently completed studies on the long-term effects of MDMA in nonhuman primates. The goals of these studies were to (1) determine if the neurotoxic effects of MDMA, which have been well documented in the rodent (see below), generalize to the primate (2) compare the relative sensitivity of primates and rodents to the neurotoxic effects of MDMA (3) ascertain if the toxic effects of MDMA in the monkey are restricted to nerve fibers (as they are in the rat), or if they involve cell bodies as well (4) evaluate how closely toxic doses of MDMA in the monkey approximate those used by humans and (5) examine whether 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) can be used to detect MDMA-induced serotonergic damage in the CNS of primates. Before presenting the results of these studies, previous results in the... [Pg.306]

Ricaurte, G.A. DeLanney, L.E. Wiener, S.G. Irwin, L and Langston, J.W. 5-Hydroxyindoleacetic acid in cerebrospinal fluid reflects serotonergic damage induced by 3,4-methylenedioxymethamphetamine in CNS of nonhuman primates. Brain Res 474 359-363. 1988b. [Pg.321]

Sanders-Bush, E. Bushing, J.A. and Sulser, F. Long-term effects of /)-chloroamphetamine on tryptophan hydroxylase activity and on the levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in brain. Eur J Pharmacol 20 385-388, 1972. [Pg.356]

HIAA, 5-hydroxyindoleacetic acid CGRP, calcitonin-gene-related peptide DOPAC, 3,4-dihydroxyphenylacetic acid ... [Pg.250]

Many of the neuropsychiatric symptoms in early hepatic encephalopathy, such as altered sleep patterns, are signs that have classically been attributed to modifications of serotoninergic neurotransmission. Serotonin turnover, as indicated by the ratio of the concentrations of the metabolite 5-hydroxyindoleacetic acid to serotonin, is increased in brain in both human and experimental hepatic encephalopathy. [Pg.597]

Serotonergic function has been investigated by using multiple methods. Assaying the major metabolite of serotonin, 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF) has been widely used (Ch. 13). This method assumes that CSF 5-HIAA is related to brain serotonin activity. This premise is supported by the rostral-caudal concentration gradient of CSF 5-HIAA and the observation in postmortem studies that CSF 5-HIAA correlates with levels of 5-HIAA in prefrontal cortex [16], both of which suggest that CSF 5-HIAA is a reasonable index of prefrontal serotonin turnover. ... [Pg.889]

EPP evoked end-plate potential 5-HIAA 5-hydroxyindoleacetic acid... [Pg.964]

A puzzling finding regarding the 5-HT syndrome is the report that the deam-inated indoles 5-hydroxyindoleacetic acid (5-HIAA the primary metabolite of 5-HT) and indoleacetic acid (IAA) are effective in producing the syndrome... [Pg.36]

Involvement of endogenous 5-HT in emesis was investigated. It was found that reserpine, p-chlorophenylalanine (PCPA) and fenfluramine antagonized cisplatin-induced emesis in the ferret [109]. The real role of 5-HT was difficult to assess, as all these agents with a possible exception of PCPA, depleted 5-HT, dopamine (DA) and noradrenaline (NE), unselectively. Cisplatin, the potent emetogenic agent, moderately increased brain levels of DA and decreased NE, while it had no significant effect on 5-HT or 5-hydroxyindoleacetic acid. [Pg.314]

Cassel GE, Koch M, Tiger G. 1995. The effects of cyanide on the extracellular levels of dopamine, 3,4,-dihydroxyphenylacetic acid, homovanillic acid, 5-hydroxyindoleacetic acid and inositaol phospholipid breakdown in the brain. Neurotoxicology 16(l) 73-82. [Pg.242]

In contrast, much is known about the catabolism of catecholamines. Adrenaline (epinephrine) released into the plasma to act as a classical hormone and noradrenaline (norepinephrine) from the parasympathetic nerves are substrates for two important enzymes monoamine oxidase (MAO) found in the mitochondria of sympathetic neurones and the more widely distributed catechol-O-methyl transferase (COMT). Noradrenaline (norepinephrine) undergoes re-uptake from the synaptic cleft by high-affrnity transporters and once within the neurone may be stored within vesicles for reuse or subjected to oxidative decarboxylation by MAO. Dopamine and serotonin are also substrates for MAO and are therefore catabolized in a similar fashion to adrenaline (epinephrine) and noradrenaline (norepinephrine), the final products being homo-vanillic acid (HVA) and 5-hydroxyindoleacetic acid (5HIAA) respectively. [Pg.97]

Mice exposed for 28 days to phenol in drinking water exhibited a significant reduction in dopamine level in the corpus striatum at the 1.8 mg/kg/day dose, and significantly decreased levels of norepinephrine, serotonin, and 5-hydroxyindoleacetic acid in the hypothalamus at the 6.2 mg/kg/day dose (Hsieh et al. 1992). Levels of neurotransmitters in other brain regions were also significantly altered at higher doses of phenol. [Pg.75]

Serotonin is an indolamine neurotransmitter, derived from the amino acid L-tryptophan. Tryptophan is converted to 5-hydroxytryptophan (5-HTP) by tryptophan hydroxylase. 5-HTP is converted to 5-hydroxytryptamine (serotonin, 5-HT) by aromatic amino acid decarboxylase. In the pineal gland, 5-HT may be further converted to /V-acetyl serotonin by 5-HT /V-acetyltransferase and then to melatonin by 5-hyroxyindole-O-methyltransferase. 5-HT is catabolized by monoamine oxidase, and the primary end metabolite is 5-hydroxyindoleacetic acid (5-HIAA). [Pg.52]

Boonen G, Ferger B, Kuschinsky K, Haberlein H. (1998). In vivo effects of the kavalactones (+)-dihydromethysticin and (H-/-)-kavain on dopamine, 3,4-dihydroxyphenylacetic acid, serotonin and 5-hydroxyindoleacetic acid levels in striatal and cortical brain regions. Planta Med. 64(6) 507-10. Boonen G, Haberlein H. (1998). Influence of genuine kavalactone enantiomers on the GABA-A binding site. Planta Med. 64(6) 504-6. [Pg.494]

Kalen P, Strecker RE, Rosengren E, Bjorklund A. 1988. Endogenous release of neuronal serotonin and 5-hydroxyindoleacetic acid in the caudate-putamen of the rat as revealed by intracerebral dialysis coupled to high-performance liquid chromatography with fluorimetric detection. J Neurochem 51(5) 1422-1435. [Pg.248]

Ruggeri M, Merlo Rich E, Zini I, Fuxe K, Ungerstedt U, et al. 1990. Indole-pyruvic acid increases 5-hydroxyindoleacetic acid levels in the cerebrospinal fluid and frontoparietal cortex of the rat a microdialysis study. Acta Physiol Scand 138(1) 97-98. [Pg.253]

HT is metabolized by the action of monoamine oxidase by a process of oxidative deamination to yield 5-hydroxyindoleacetic acid (5-HIAA). In the pineal gland, 5-HT is o-methylated to form melatonin. While the physiological importance of this transmitter in the regulation of the oestrus cycle in ferrets would appear to be established, its precise role in man is unknown. Nevertheless, it has been speculated that melatonin plays some... [Pg.71]

Colorimetric assays used in endocrinological procedures are also often subject to drug interference. We have observed an interesting interference in a patient with carcinoid. The patient excreted 400 mg of 5-hydroxyindoleacetic acid (5-HIAA) and when a vanillylmandclic acid (VMA) determination was performed by a nonspecific diazo method, the value was reported to be 375 mg. The catecholamines were just above normal. There was an immediate suggestion that the patient also had a pheochromocytoma. However, when a specific chromatographic VMA method was used, the value was found to be within normal limits. Subse-... [Pg.31]

Nielsen DA, Goldman D, Virkkunen M, Tokola R, Rawlings R, Linnoila M (1994) Suicidality and 5-hydroxyindoleacetic acid concentration associated with a tryptophan hydroxylase polymorphism. Arch Gen Psychiatry 51 34-38 Nielsen DA, Virkkunen M, Lappalainen J, Eggert M, Brown GL, Long JC, Goldman D, Linnoila M (1998) A tryptophan hydroxylase gene marker for suicidality and alcoholism. Arch Gen Psychiatry 55 593-602... [Pg.109]


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5-Hydroxyindoleacetic acid 5- HIAA

5-Hydroxyindoleacetic acid assay

5-Hydroxyindoleacetic acid excretion

5-Hydroxyindoleacetic acid formation

5-Hydroxyindoleacetic acid/5-Hydroxyindoleacetate

5-Hydroxyindoleacetic acid/5-Hydroxyindoleacetate

5-hydroxyindoleacetate

Plasma 5-hydroxyindoleacetic acid

Serotonin 5-hydroxyindoleacetic acid level

Urine 5-hydroxyindoleacetic acid

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