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PubMed1991

Effect of tryptophan on extracellular concentrations of tryptophan and 5-hydroxyindoleacetic acid in the striatum and cerebellum.

The effects of L-tryptophan (50 mg/kg i.p.) on extracellular concentrations of tryptophan and the 5-hydroxytryptamine (5-HT) metabolite 5-hydroxyindoleacetic acid (5-HIAA) were determined in the rat striatum and cerebellum, regions with rich and poor 5-HT innervation, respectively. Determinations were on perfusates from dialysis probes in the brains of conscious, freely moving rats. The pharmacokinetic profiles of dialysate tryptophan after tryptophan load (peak concentration, time to peak concentration, area under curve, and half-life) in the two regions did not differ significantly. The dialysate 5-HIAA concentration in the striatum rose two- to threefold after the administration of tryptophan. Therefore, as 5-HIAA was undetectable in the cerebellum either before or after the administration of tryptophan, the increase of 5-HIAA in the striatum is unlikely to depend appreciably on its production within the cerebral vasculature or outside the brain or on its entering the striatum through a blood-brain barrier damaged by placement of the dialysis probe. Overall, the findings strengthen previous evidence that extracellular 5-HIAA concentrations determined by cerebral dialysis are a valid measure of the metabolism of 5-HT of brain neuronal origin.

Animals↗

PubMed1983

Drug-induced alterations in the efflux of 5-hydroxytryptamine and of 5-hydroxyindoleacetic acid into superfusates of the rat spinal cord.

The effect of dl-p-chloroamphetamine, fluoxetine and probenecid on the efflux of endogenous 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acid (5HIAA) into superfusates of the spinal cord of anesthetized rats was examined. Mean basal efflux of 5HT and 5HIAA was 0.27 and 15.56 ng/ml superfusate, respectively. The addition of dl-p-chloroamphetamine to the superfusate produced a dose-dependent increase in the efflux of 5HT into the superfusate, but did not increase the efflux of 5HIAA. Probenecid (200 mg/kg i.p.) increased the basal efflux of both 5HT and 5HIAA as compared to control values. When administered systemically, fluoxetine (10 mg/kg i.p. or s.c.) decreased the basal efflux of 5HIAA, but did not alter the basal efflux of 5HT as compared to control values. In contrast, when administered in the superfusate, fluoxetine produced a dose-dependent increase in the basal efflux of 5HT, but did not alter the basal efflux of 5HIAA. The release of 5HT produced by the addition of 2.5 X 10(-4) M dl-p-chloroamphetamine to the superfusate was not prevented in rats pretreated systemically with fluoxetine, although when administered in the superfusate fluoxetine inhibited the dl-p-chloroamphetamine-induced release of 5HT.

Animals↗

PubMed1981

Distribution of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in human brain in relation to age, drug influence, agonal status and circadian variation.

The post-mortem brain concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined in 16 parts of the brain from patients with no history of neurologic, psychiatric or metabolic illness. The causes of death were either ischemic heart disease, infections disease, cancer or accidents. Forty-two men with a mean age of 57 years (range 18-95 years) and 19 women with a mean age of 62 years (range 23-79 years) were included. The influence of several factors were studied: brain weight, time between death and autopsy, storage time before chemical analysis, age, sex, agonal status, cerebral arteriosclerosis, cancer, opiate treatment and time of death during the day. Most correlations between the 5-HT concentrations in different brain parts were positive, the strongest correlations in the basal ganglia and the limbic system. No consistent pattern of age-related 5-HT changes were found. The females had significantly higher 5-HIAA concentrations in the cortex of the gyrus hippocampus. Final hypoxia seemed to decrease 5-HT concentrations. Opiate treatment reduced 5-HT and increased 5-HIAA concentrations. A marked circadian variation of 5-HT was found, most pronounced in the hypothalamus, the limbic system and some neocortical areas.

Adolescent↗

PubMed1989

Patterns of extracellular 5-hydroxyindoleacetic acid (5-HIAA) in the paraventricular hypothalamus (PVN): relation to circadian rhythm and deprivation-induced eating behavior.

Daily rhythms in extracellular levels of the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were examined in the region of the paraventricular nucleus (PVN), using intracerebral microdialysis combined with high performance liquid chromatography and electrochemical detection. Samples of PVN dialysate, from 11 rats on a 12/12 hr light/dark cycle, were collected and assayed for 5-HIAA every 2 hr for 3 days. During the first 2 days the rats were given free access to food. During the 3rd day they were deprived of food for a 24-hr period and then given food for 4 hr. The results showed that in freely-feeding rats, there was a 24-hr rhythm in the levels of 5-HIAA, with a marked transient peak just after the beginning of the dark portion of the light/dark cycle and stable levels at all other times. When the animals were food-deprived, PVN levels of this metabolite remained stable, and the early dark peak was abolished, suggesting that it might have been consequent to the eating behavior which normally occurred at this time. In the 4-hr refeeding period, there were no changes in 5-HIAA levels, despite the intense eating behavior which occurred during this time. These patterns of 5-HIAA in the PVN region, taken together with previous evidence, suggest that PVN serotonin metabolism may increase in association with feeding specifically in the early portion of the nocturnal eating period, when it may play a role in controlling food intake and macronutrient selection.

Animals↗

PubMed1996

In-vivo microdialysis measurement of 5-hydroxytryptamine and its metabolites, 5-hydroxyindoleacetic acid and N-acetyl 5-hydroxytryptamine, in rat blood: effects of histamine-receptor antagonists.

The blood concentrations of 5-hydroxytryptamine (5-HT) and its metabolites, 5-hydroxyindoleacetic acid (5-HIAA) and N-acetyl 5-HT were assayed by in-vivo microdialysis and a highly sensitive HPLC procedure that was originally developed to analyse CNS mediators. We investigated the effects of histamine-receptor antagonists on 5-HT metabolism and its release into the blood of rats. The mean basal levels of 5-HT, 5-HIAA and N-acetyl 5-HT in the blood measured by in-vivo microdialysis were 77.2 +/- 9.4, 20.3 +/- 1.5 and 1.89 +/- 0.15 pmol mL-1, respectively. These levels were not significantly affected by an intraperitoneal injection of saline, and remained at constant levels for at least 8 h after administration of saline. After an intraperitoneal injection of 5-HT hydrochloride (0.5 mg kg-1), 5-HT was soon detected in the blood of the jugular vein. 5-HIAA also quickly appeared in the blood and declined monoexponentially from 60 min after injection. In contrast, N-acetyl 5-HT slowly appeared in the blood and it reached a maximal level at 270 min. The 5-HT and N-acetyl 5-HT levels in dialysates from rat jugular vein were significantly increased by intraperitoneal pyrilamine (2.0 mg kg-1), (+)-chlorpheniramine (2.0 mg kg-1) and cimetidine (20.0 mg kg-1). However, there was no increase in the 5-HIAA concentration after an intraperitoneal injection of these histamine-receptor antagonists, demonstrating that the 5-HT released from various cells containing 5-HT was predominantly metabolized to N-acetyl 5-HT by N-acetyltransferase. Moreover, thioperamide did not affect the basal levels of 5-HT, 5-HIAA or N-acetyl 5-HT. Because the recovered 5-HT, 5-HIAA and N-acetyl 5-HT in the dialysate is directly proportional to the free fraction in the blood, in-vivo microdialysis is a reliable method of examining 5-HT metabolism and its release into the blood.

Animals↗

PubMed1982

Effect of omental transposition on to the brain on the cortical content of norepinephrine, dopamine, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in experimental cerebral ischaemia.

Local cerebral ischaemia causes a significant decrease in norepinephrine, dopamine, 5-hydroxytryptamine in the cortical brain tissue of rabbits, associated with an increase in 5-hydroxyindoleacetic acid. Previous transposition of the omentum on to the brain surface maintains, to a large extent, physiological levels of these metabolites. This study stresses the role of the transposed omentum in reducing the effects of experimental occlusion of a major cerebral artery.

Animals↗

PubMed1988

Determination of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in plasma by direct injection in coupled-column liquid chromatography with electrochemical detection.

A method is described that allows determination of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in platelet-poor human blood plasma after direct injection of 50-100 microliters of plasma into a coupled-column liquid chromatographic system. The chromatographic system comprised an enrichment column and two separation columns with different selectivity properties. The samples were injected into the C18 enrichment column, which was eluted with a buffer solution as the mobile phase. 5-HT, 5-HIAA and the internal standard 5-hydroxy-N-methyl-tryptamine (5-HMT) were then desorbed by a stronger mobile phase and flushed into a cation exchanger, which separated 5-HT and 5-HMT. 5-HIAA passed straight through and was switched to a C18 column where it was retarded. After 5-HT and 5-HMT had been eluted from the cation exchanger and detected, the eluate from the C18 column was directed to the detector and 5-HIAA was determined. Basic plasma levels, about 4 nM for 5-HT and 30 nM for 5-HIAA, were measured with a relative standard deviation of about 5%.

Animals↗

PubMed1995

The association of urinary 5-hydroxyindoleacetic acid and vanillylmandelic acid in patients with generalized anxiety.

There is evidence that serotonin and norepinephrine are in some way involved in the pathophysiology of anxiety disorders. Urinary levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and the norepinephrine metabolite vanillylmandelic acid (VMA) were measured in 46 patients with generalized anxiety disorder. There was a significant association between urinary levels of 5-HIAA and VMA: r = 0.79; p = 0.0001. Possible implications of this finding are discussed.

Anxiety Disorders↗

PubMed1988

[Opposite variations of extracellular concentrations of 5-hydroxyindoleacetic acid (5-HIAA) measured by voltammetry of axonal terminals and cell bodies of the dorsal raphe nucleus through the sleep-wake cycle].

Differential pulse voltammetry was used for 5-hydroxyindoleacetic acid (5-HIAA) detection in the rat caudate (n. Cd) and Raphe Dorsalis (n. RD) nuclei, in chronic experimental conditions. In the anterior and ventral part of n. RD, large increases in the extracellular concentrations of 5-HIAA were reported during slow wave sleep (SWS) and paradoxical sleep (PS) whereas a decrease occurred during waking. These variations could reflect the dendritic release of serotonin. In n. Cd, opposite variations of the extracellular concentrations of 5-HIAA were observed i.e. increase during waking state and decrease during SWS and PS.

Animals↗

PubMed1987

5-Hydroxytryptophol and 5-hydroxyindoleacetic acid levels in rat brain: effects of various drugs affecting serotonergic transmitter mechanisms.

The effect of various pharmacological treatments on the levels of free and total 5-hydroxytryptophol (5-HTOL) and 5-hydroxyindoleacetic acid (5-HIAA) in rat brain were investigated using a gas chromatographic-mass spectrometric technique. The disappearance of 5-HTOL following monoamine oxidase (MAO) inhibition induced by pargyline was more rapid (t1/2 10-15 min) than that of 5-HIAA (t1/2 30-40 min) in all regions investigated, indicating a rapid turnover of 5-HTOL. The selective MAO-A inhibitor chlorgyline produced a more pronounced reduction of 5-HTOL than of 5-HIAA, while the MAO-B inhibitor deprenyl was without effect on both serotonin metabolites. The MAO-A inhibitor amiflamine which is selective for serotonin neurons, was also more effective in reducing free 5-HTOL levels than of 5-HIAA levels, suggesting that the formation of 5-HTOL is closely associated with serotonin neurons. Neonatal treatment with the serotonin neurotoxin 5, 7-dihydroxytryptamine (5,7-HT) led to a more pronounced reduction of 5-HTOL levels in cerebral cortex than that of 5-HIAA levels, while the increase of 5-HTOL levels in pons-medulla was more marked than of 5-HIAA levels. Probenecid treatment increased several fold both conjugated 5-HTOL and 5-HIAA levels in brain tissue. An increase was also noted for free 5-HTOL, although of less magnitude. Treatment with the serotonin receptor active agents methiothepin and d-lysergic acid diethylamide produced similar alterations of free 5-HTOL and 5-HIAA. The present results have demonstrated that free 5-HTOL has a rapid turnover in rat brain and that free 5-HTOL levels may serve as a useful index for serotonin turnover.

Animals↗

PubMed1982

Factors influencing melatonin, 5-hydroxytryptophol, 5-hydroxyindoleacetic acid, 5-hydroxytryptamine and tryptophan in rat pineal glands.

Using a simple high performance liquid chromatographic method, we measured melatonin, N-acetyl-5-hydroxytryptamine (NAc-5HT), 5-hydroxytryptophol (5HTOL), 5-hydroxyindoleacetic acid (5HIAA), 5-hydroxytryptamine (5HT) and tryptophan in single rat pineal glands. 5-Methoxytryptophol and 5-methoxyindoleacetic acid were not detected at levels which have been reported previously. 5HTOL, 5HIAA and 5HT showed the opposite diurnal rhythm to NAc-5HT and melatonin. Light during the dark period lowered melatonin while increasing 5HTOL, 5HIAA and 5HT. As the peak 5HTOL levels were higher than the peak melatonin levels, the functional significance of 5HTOL deserves consideration. Tryptophan administration increased melatonin and 5HTOL as well as the other indoles.

Animals↗

PubMed1983

REM sleep eye movement activity and CSF concentrations of 5-hydroxyindoleacetic acid in psychiatric patients.

The relationship between rapid-eye-movement (REM) sleep tonic and phasic activity measures and the pre- and postprobenecid cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) was examined in a sample of 14 unmedicated psychiatric patients. The average duration of an eye movement burst and the average number of eye movements within a burst were found to be inversely related to the probenecid corrected accumulation of 5-HIAA in the CSF. These results are interpreted as indicating an association between REM burst eye movement activity and serotonin turnover in psychiatric subjects.

Adult↗

PubMed1984

The urinary excretion of 5-hydroxyindoleacetic acid does not reflect brain levels of this metabolite of 5-hydroxytryptamine.

The present study was undertaken to determine if changes in the serotonergic central nervous system can be reflected by urinary 5-hydroxyindoleacetic acid (5-HIAA) levels. Cerebral, spinal and urinary levels of 5-HIAA were determined and compared in rats whose cerebral 5-HIAA concentration had been depleted by nucleus raphe dorsalis and medialis lesion or increased by L-tryptophan loading. Since no differences were observed in the urinary excretion of 5-HIAA we conclude that this parameter cannot be used to detect changes in the serotonergic central nervous system.

Animals↗

PubMed1994

Simultaneous determination of tryptophan, 5-hydroxytryptophan, 5-hydroxytryptamine, 5-hydroxyindoleacetic acid, 4-hydroxy-3-methoxyphenylacetic acid and 3-methoxy-4-hydroxyphenylglycol in human cerebrospinal fluid.

Serotonin (5-hydroxytryptamine) metabolism may be influenced by its precursor tryptophan. A method utilizing reversed-phase high-performance liquid chromatography and electrochemical and ultraviolet detection with a mobile phase composed of acetate buffer and methanol has been developed for determination of tryptophan, its metabolites 5-hydroxytryptophan, serotonin, 5-hydroxyindoleacetic acid, as well as 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid) and 3-methoxy-4-hydroxyphenylglycol in human cerebrospinal fluid (CSF). The electrochemical potential is set at 0.6 V in order to reduce the background current. Since tryptophan is not electroactive at this potential, it is detected by ultraviolet absorbance. The present method is simple, rapid, specific and accurate as compared with a previously reported method. No sample pretreatment is necessary and it takes ca. 20 min to run a sample. The concentrations of the compounds measured in CSF are similar to those obtained by HPLC in previous reports, although there are still arguments about the true level of serotonin in CSF.

5-Hydroxytryptophan↗

PubMed1991

Effects of d- and dl-chlorpheniramine on serotonin and 5-hydroxyindoleacetic acid levels in the regional parts of rat brain.

The purpose of this study was to further investigate the effects of chlorpheniramine (d- and dl-forms) on the levels of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the regional parts of rat brain. After the intravenous administration of each form of chlorpheniramine, the 5-HT and 5-HIAA levels were measured by HPLC system. Each form of chlorpheniramine is effective in reducing 5-HIAA, but not 5-HT levels in most of the regional brain of rats. The degree of reducing 5-HIAA levels does not correlate with the antihistaminic potency of these drugs. Our previous results showed that chlorpheniramine reduced the 3,4-dihydroxyphenylacetic acid levels, but not the dopamine levels in the brain of rats. Taken together, these findings raise problems regarding possible physiological and behavioral effects by using chlorpheniramine as a histamine H1-blocker in animal experiments.

Animals↗

PubMed1993

Circadian variation in plasma 5-hydroxyindoleacetic acid level during and after alcohol withdrawal: phase advances in alcoholic patients compared with normal subjects.

Alcohol withdrawal symptoms in 19 male alcoholics were objectively evaluated and classified and circadian variation in their plasma 5-hydroxyindoleacetic acid (5-HIAA) concentrations was determined at 3 different intervals after cessation of drinking. Circadian variations in plasma 5-HIAA level exhibited phase advances in alcoholic patients compared with normal controls and were different depending on the severity of alcohol withdrawal symptoms. Plasma 5-HIAA in patients with delirium tremens showed significantly higher levels during the abstention period, possibly suggesting peculiarity in their serotonergic metabolism.

Adult↗

PubMed1981

Determination of 5-hydroxyindoleacetic acid in urine by high-performance liquid chromatography: a fully automated method.

High-performance liquid anion-exchange chromatography is combined with continuous flow spectrofluorometry at an optimized pH for the determination of 5-hydroxyindoleacetic acid (5-HIAA) in urine. Its chief advantages are speed (7 min per determination), enabling measurement of large series of samples, precision (coefficient of variation = 0.72%), sensitivity (detection limit: 1 pmol) and specificity (no interference with 5-HIAA precursors or with the drugs tested). Reference values (n = 112) are 25 +/- 25 mumol per 24 h. Comparison with a reference spectrofluorometric technique shows a correlation coefficient of 0.96.

Automation↗

PubMed1995

Effect of probenecid on 5-hydroxyindoleacetic acid in cisternal cerebrospinal fluid of rats with portacaval anastomosis.

Portal-systemic encephalopathy (PSE) is characterized by a neuropsychiatric disorder progressing through personality changes, to stupor and coma. Previous studies have revealed alterations of serotonin and of its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in brain tissue and CSF in experimental (rat) and human PSE. Increased brain 5-HIAA concentrations could result from its decreased removal rather than to increased serotonin metabolism. In order to evaluate this possibility, CSF 5-HIAA concentrations were measured using an indwelling cisterna magna catheter technique at various times following end-to-side portacaval anastomosis in rats (the most widely used animal model of PSE) treated with probenecid, a competitive inhibitor that blocks the active transport of acid metabolites out of the brain and CSF. Following portacaval anastomosis and probenecid treatment, CSF concentrations of 5-HIAA were increased to a greater extent than in sham-operated controls. When data were expressed as per-cent baseline values, the relative increase of CSF 5-HIAA in portacaval shunted rats following probenecid treatment was not significantly different from sham-operated controls. These findings confirm that increased 5-HIAA in the CNS in experimental PSE results from increased 5HT metabolism or turnover and that the probenecidsensitive acid metabolite carrier is intact in PSE.

Animals↗