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PubMed1992

[Effect of acute and chronic administration of L- thyroxine and methimazole on blood levels of tryptophane, serotonin and 5-hydroxyindoleacetic acid in plasma of rats].

The effects of hyperthyreosis induced by the administration of thyroxine and hypothyreosis induced by the administration of methimazole on the levels of tryptophane, serotonin and 5-hydroxyindoleacetic acid in low-platelet blood plasma have been studied in Wistar rats. Thyroxine administration (120 micrograms/kg/24 h, intraperitoneally) lasting 7 days caused a decrease in serotonin concentration by 38 per cent. The level of this amine in rats receiving thyroxine during three months was elevated by almost three times. Tryptophane concentration did not change following thyroxine administration. Methimazole administration lasting 14 days (oral dose 15 mg/kg/24 h) caused an increase in tryptophane concentration by 34 per cent and in serotonin concentration by 24 per cent. Long-term hypothyreosis induced by methimazole administration lasting three months caused an 39 per cent increase in tryptophane and 38 per cent increase in serotonin concentration. Neither hyperthyreosis induced by thyroxine administration nor hypothyreosis induced by methimazole++ caused any changes in the concentration of 5-hydroxyindoleacetic acid. The importance of serotonin in pathogenesis of clinical symptoms accompanying the states of deficit or excess of thyroid hormones needs further elucidation.

Animals↗
PubMed1976

Concentration of 5-hydroxyindoleacetic acid, homovanillic acid, and tryptophan in the cerebrospinal fluid of depressed patients before and after ECT.

Cerebrospinal fluid (CSF) levels of 5-hydroxyindoleacetic acid (5HIAA), tryptophan (TRYP), and homovanillic acid (HVA), were determined prior to electroconvulsive therapy (ECT) and after an average course of 6.7 ECT in six endogenous depressed patients. Depression rating scale (DRS) scores were also obtained by a "blind" research psychiatrist before and after ECT at the time of each lumbar puncture. ECT markedly reduced DRS scores but did not significantly alter CSF levels of 5HIAA, TRYP, or HVA. We found no correlation between ECT-induced DRS score reductions and changes in any of the CSF constituents studied, or between the absolute DRS score and the corresponding CSF concentration of any of the compounds. These data are consistent with those previously reported for ECT and do not suggest that ECT alters cerebral amine metabolism in depressed patients. Neither do they provide any evidence for direct amine mediation of the depression-relieving effects of ECT in man, nor for any relation between severity of depressive illness and CSF concentrations of 5HIAA, TRYP, or HVA.

Adult↗
PubMed1984

Five antidepressant treatments in depressed patients. Effects on urinary serotonin and 5-hydroxyindoleacetic acid output.

The 24-hour urinary serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) outputs were repeatedly measured in 21 patients with major affective disorders after a minimum of three weeks free of drug treatments and at steady state during subsequent antidepressant treatments or during the second week after a series of electroconvulsive treatments (ECTs). The 5-HIAA outputs were more variable over time than the outputs of major catecholamine metabolites, previously studied by us. Patients with rapid mood cycles excreted large amounts of 5-HT. Lithium carbonate and ECTs reduced the outputs of 5-HT and 5-HIAA, respectively. Lithium carbonate also stabilized the output of 5-HT. No common effect of different antidepressant treatments on indole outputs was found.

Antidepressive Agents↗
PubMed1978

The effect of lithium on the increase in forebrain 5-hydroxyindoleacetic acid produced by raphe stimulation.

1 The change in forebrain 5-hydroxyindoleacetic acid (5-HIAA) concentration induced by raphe stimulation has been studied in rats treated with Li+ or 0.9% w/v NaCl solution (saline) for 10 days. 2 Raphe stimulation increased the forebrain concentration of 5-HIAA in both groups of animals. Chlorimipramine abolished this effect in the control group, but not in the Li+ group. 3 The inhibition of 5-hydroxytryptamine (5-HT) uptake by chlorimipramine was not affected by pretreatment with Li+ or by the addition of Li+ to synaptosomal suspensions in vitro. 4 It is suggested that the production of 5-HIAA following raphe stimulation in Li+-treated animals is derived from the metabolism of 5-HT which remains within the intracellular environment. The consequence of this in relation to transmitter release is discussed.

Animals↗
PubMed1983

Concentrations of 5-hydroxyindoleacetic acid and homovanillic acid in the cerebrospinal fluid of chronic therapy-resistant schizophrenics before and after hemodialysis therapy.

The concentrations of the monoamine metabolites 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) have been determined by high-performance liquid chromatography in samples of lumbar cerebrospinal fluid from chronic therapy-resistant schizophrenics, both before and after either inactive or active hemodialysis for 10 weeks. A reasonable test-retest reliability was found for 5-HIAA during the inactive dialysis, but this was not found during active dialysis.

Adult↗
PubMed1978

Alterations of cerebrospinal fluid 5-hydroxyindoleacetic acid, and total blood serotonin content during clozapine treatment.

Cerebrospinal fluid 5-hydroxyindoleacetic acid level, and total blood serotonin content was measured in groups of manic and schizophrenic patients before and after 2, 4, 6, 10, 20, and 30 days of clozapine treatment. CSF 5-HIAA values were elevated after 2 and 4 days and returned to baseline levels after 6 days or more. Blood serotonin content, in contrast, increased gradually and remained high even after 30 days. Neither CSF 5-HIAA nor blood 5-HT correlated with age, drug dose, or clinical effectiveness, but some relationship between these and the sedative component of the clozapine action was observed.

Adult↗
PubMed1982

Urinary excretion of 5-hydroxyindoleacetic acid--no relationship to the level in cerebrospinal fluid.

Concentrations of 5-hydroxyindoleacetic acid (5-HIAA) were determined in urine and cerebrospinal fluid (CSF) by mass fragmentography. A pronounced day-to-day variation in the urinary excretion of 5-HIAA was found both in psychiatric patients and a healthy control. Lumbar punctures performed twice 3-12 weeks apart in 11 healthy controls resulted in reproducible levels of 5-HIAA in CSF (r = 0.89; P less than 0.001). The mean of three periods of daily 5-HIAA excretion was not correlated to the CSF level measured in 18 psychiatric patients (r = 0.09). Three weeks of chlorimipramine treatment significantly decreased CSF 5-HIAA levels (P less than 0.05), but not the urinary excretion of 5-HIAA. It might be concluded that measurement of urinary 5-HIAA excretion is of little value compared to CSF levels in studies of serotonin in the central nervous system.

Clomipramine↗
PubMed1984

Measurement of 5-hydroxytryptophol and 5-hydroxyindoleacetic acid in human and rat brain and plasma.

The levels of 5-hydroxyindoleacetic acid (5-HIAA) and free and total 5-hydroxytryptophol (5-HTOL) in human and rat brain regions and plasma were determined by a specific capillary column gas chromatographic--mass spectrometric method. The human brains were obtained 2-3 hours post mortem, and the levels of 5-HIAA were in the range of 0.48-31.3 nmoles/g in the regions investigated. The levels of free and total 5-HTOL were 10.9-387 pmoles/g and 14.5-821 pmoles/g, respectively. The ratio of total 5-HTOL to 5-HIAA was in the range of 0.6-5.5%. In human plasma the levels of free and total 5-HTOL were 0.9 +/- 0.3 and 2.9 +/- 0.8 pmoles/ml +/- S.E.M., respectively. In regions of rat brain, the 5-HIAA levels ranged from 0.37-2.84 nmoles/g. Free and total 5-HTOL were in the range of 11.4-56.1 and 16.2-77.1 pmoles/g, respectively. The ratio of total 5-HTOL and 5-HIAA ranged from 2.3-5.1%. Higher levels of 5-HIAA and 5-HTOL occurred in the rat pineal gland. In rat plasma the levels of free and total 5-HTOL were 1.34 +/- 0.06 and 21.6 +/- 1.6 pmoles/ml +/- S.E.M., respectively.

Aged↗
PubMed1982

Simultaneous measurement of dopamine and its metabolites, 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and tryptophan in brain tissue using liquid chromatography and electrochemical detection.

An assay has been developed for brain tryptophan using reverse-phase liquid chromatography with electrochemical detection. The method simultaneously assays dopamine (DA) and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), as well as 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA). The method does not require elution from ion exchange resins. After deproteinization and centrifugation samples are injected directly onto the chromatographic column. It was found that small changes in mobile phase pH markedly influenced the retention time of tryptophan while elution of the indoleamines and catecholamines did not change. The assay of these endogenous compounds in a single injection proved not expedient but inexpensive. Values obtained using alumina and ion exchange resins yielded comparable values.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Serotonin content of foods: effect on urinary excretion of 5-hydroxyindoleacetic acid.

Using a highly specific radioenzymatic assay we determined the serotonin concentration in 80 types of foods. The following fruits had a high serotonin concentration (mean +/- SEM) expressed in micrograms/g weight: plantain 30.3 +/- 7.5; pineapple 17.0 +/- 5.1; banana 15.0 +/- 2.4; Kiwi fruit 5.8 +/- 0.9; plums 4.7 +/- 0.8; and tomatoes 3.2 +/- 0.6. Only nuts in the walnut or hickory family had a high serotonin concentration expressed in micrograms/g weight; butternuts 398 +/- 90; black walnuts 304 +/- 46; English walnuts 87 +/- 20; shagbark hickory nuts 143 +/- 23; mockernut hickory nuts 67 +/- 13; pecans 29 +/- 4; and sweet pignuts 25 +/- 8. Ingestion of these fruits and nuts resulted in an increase in urinary 5-hydroxyindoleacetic acid excretion with no change in platelet serotonin concentration. The above foods should not be eaten while a urine is being collected for 5-hydroxyindoleacetic acid analysis.

Adult↗
PubMed2004

5-Hydroxyindoleacetic acid and homovanillic acid concentrations in cerebrospinal fluid in patients with Alzheimer's disease, depression and mild cognitive impairment.

In this study we investigated the cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) in Alzheimer (AD) patients (n=75), patients with mild cognitive impairment (MCI, n=9) and patients with depression (n=7). CSF HVA was significantly elevated in AD with depression (Geriatric Depression Scale, 15 point version GDS>5) in comparison to AD without depression (p<0.05, ANOVA) and CSF HVA showed a significant positive correlation with the GDS score of AD-patients (p=0.03, Spearman Rho: 0.38, Spearman Rank Correlation). In the group of AD patients CSF 5-HIAA was positively correlated with cerebrospinal fluid beta-amyloid 1-42 (Abeta42), p<0.05, Spearman Rho: 0.3, Spearman Rank Correlation, but not with CSF tau. Additionally, there was a significant positive correlation between cerebrospinal fluid 5-HIAA and HVA in the group of AD patients (p<0.0001, Rho: 0.47, Spearman Rank correlation). Neither 5-HIAA nor HVA in CSF could differentiate between mild cognitive impairment, depression and AD. The results of this study support the hypothesis that the serotonergic system plays a role in the course of AD. They further suggest an important role of dopamine metabolism in depression within AD patients.

Aged↗
PubMed1983

Low CSF 5-hydroxyindoleacetic acid in schizophrenic patients with enlarged cerebral ventricles.

The authors assayed CSF 5-hydroxyindoleacetic acid (5-HIAA) concentrations in 24 chronic schizophrenic patients, 9 of whom had enlarged cerebral ventricles according to computerized tomography scans, and in 15 control subjects with neurological disorders. Although there were no overall differences between the schizophrenic patients and the control subjects, schizophrenic patients with enlarged ventricles had significantly lower 5-HIAA concentrations. Also, ventricular size correlated inversely with 5-HIAA concentrations. The findings are consistent with other evidence that cerebral ventricular size is biologically meaningful in schizophrenic patients.

Adult↗
PubMed1988

Changes in plasma and brain tryptophan and brain serotonin and 5-hydroxyindoleacetic acid after footshock stress.

Brain concentrations of tryptophan, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) and plasma amino acids were measured after 15 or 30 minutes of intermittent footshock. Footshock treatment significantly decreased the content of 5-HT in prefrontal cortex and hypothalamus, but not brainstem at 15 min, but the decreases were reversed by 30 min. 5-HIAA, the major catabolite of 5-HT, increased in prefrontal cortex after 15 min, and in prefrontal cortex and hypothalamus after 30 min footshock. 5-HIAA:5-HT ratios were increased at both timepoints in all three brain regions. Concomitant changes in the ratios of 3,4-dihydroxyphenylacetic acid (DOPAC) to dopamine and 3-methoxy,-4-hydroxyphenylethyleneglycol (MHPG) to norepinephrine were also observed. Brain concentrations of tryptophan increased progressively during the footshock in all three brain regions. Plasma concentrations of both tryptophan and tyrosine were also significantly increased, while those of histidine and lysine were decreased. It is possible that the stress-related changes in 5-HT metabolism are due to increased plasma tryptophan, in turn causing increased brain tryptophan and 5-HT synthesis. However, the transient decreases in 5-HT suggest a footshock-induced increase of 5-HT release, depleting existing stores of 5-HT, that are replenished by the increased systemic availability of tryptophan.

Animals↗
PubMed1989

Systemic endotoxin increases L-tryptophan, 5-hydroxyindoleacetic acid, 3-hydroxykynurenine and quinolinic acid content of mouse cerebral cortex.

Systemic infections and injection of endotoxin are known to increase L-tryptophan release from skeletal muscle and increase systemic L-tryptophan catabolism through the kynurenine pathway. To investigate the effects of systemically administered endotoxin on brain L-tryptophan metabolites. C57BL6/6NCR mice were given an intraperitoneal injection of 10 micrograms of lipopolysaccharide from Salmonella abortus equii and samples of serum and cerebral cortex collected. After 9 h, serum L-tryptophan concentration was decreased by 51%. At 9 h and 24 h, increases in L-tryptophan metabolites in cerebral cortex were: L-tryptophan, 42% and 39%; 5-hydroxyindoleacetic acid, 38% and 67%; 3-hydroxykynurenine, 235% and 381%; and quinolinic acid, 76% and 306%. Cortical quinolinic acid concentration was still elevated at 48 h (88%) and 72 h (79%) after lipopolysaccharide. No significant changes in cortical serotonin concentrations were found at the time points examined. When L-tryptophan (0.37 mmol/kg) was administered systemically to either normal or lipopolysaccharide-treated mice, increases in cortical L-tryptophan, serotonin, 5-hydroxyindoleacetic acid and 3-hydroxykynurenine concentrations were largest in mice treated with both lipopolysaccharide and L-tryptophan. These results suggest that disturbances in L-tryptophan metabolism that follow systemic endotoxin administration extend to the central nervous system. The consequences of these changes in L-tryptophan metabolites remain to be determined.

Animals↗
PubMed1987

Urinary excretion of 5-hydroxyindoleacetic acid, delta-aminolevulinic acid and coproporphyrin isomers in rats and men exposed to lead.

The urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA), delta-aminolevulinic acid (ALA) and coproporphyrin (CP) isomers (I and III) was investigated in rats and workers exposed to lead. Urinary excretion of 5-HIAA, which is the major metabolite of serotonin, was not influenced by the lead exposure. However, a significant increase in urinary ALA and CP was found in rats and workers exposed to lead. In particular, the urinary excretion of CP-III was markedly increased compared to that of CP-I in rats and workers exposed to lead.

Administration, Oral↗
PubMedDate not supplied

5-Hydroxyindoleacetic acid in cerebrospinal fluid in alcoholic patients under different clinical conditions.

Levels of 5-hydroxyindoleacetic acid, 5-HIAA, the main serotoninergic metabolite in the central nervous system, were investigated in the cerebrospinal fluid, CSF, of male alcoholics and healthy controls. During intoxication, 5-HIAA correlated positively to blood ethanol concentration and levels gradually decreased by length of abstinence. In patients investigated after three months of alcohol abstinence, subnormal levels were noted. Assuming that the level of 5-HIAA in the CSF reflects central serotoninergic activity, the results support the assumption of subnormal activity in abstinent alcoholics and an activation during abuse.

Alcoholism↗
PubMed1978

Exchange of 5-hydroxyindoleacetic acid between the spinal cord and lumbar cerebrospinal fluid.

1. After inhibition of 5-hydroxyindoleacetic acid (5-HIAA) transport by repeated administration of probenecid in cats, this acid accumulates linearly in the lumbosacral cord, lumbar cerebrospinal fluid (c.s.f.) and cisternal fluid during 5 hr of experiment. 2. A simple mathematical analysis of these results shows that (a) the rates of 5-HIAA accumulation in the lumbar c.s.f. and cisternal c.s.f. are faster than in the cord, (b) about 22% of 5-HIAA formed in the cord diffuses into lumbar c.s.f. and (c) by measuring 5-HIAA in the lumbar c.s.f. the concentration and turnover of 5-HIAA and turnover of serotonin in the lumbosacral cord can be calculated as well as the changes of 5-HIAA in the cisternal c.s.f. predicted. 3. These results suggest that it is possible to calculate the level and turnover of endogenous substances in the central nervous system on the basis of their measurement in the c.s.f.

Animals↗