Plasma Tryptophan and 5‐ht Metabolism in the CNS of the Newborn Rat

Bourgoin, S.; Faivre-Bauman, A.; Benda, P; Głowiński, J.; Hamon, Michel

doi:10.1111/j.1471-4159.1974.tb04361.x

Cited by 85 publications

(36 citation statements)

References 25 publications

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“…tryptophanan hydroxylase, 5-hydroxytryptophan-decarboxylase) approa ches the adult level at birth. However, per haps because of a turnover rate in the neo nate which surpasses that in the adult, trypto phan injection (100 mg/kg) in our studies caused only a slight increase in the 5-HT of neonatal brain [2,36], In addition, L-tryptophan administration did not influence the swimming ability of newborns. However, be ginning with the 3rd postnatal day, when this amino acid precursor has been reported to in crease brain 5-HT content dramatically, in jection of 100 mg/kg of tryptophan resulted in a shortened latency to swimming and increas ed number of FS.…”

Section: Discussionmentioning

confidence: 97%

“…catecholaminergic and serotonergic neuronal system in the neonatal rat brain are at differMorphological and biochemical evidence ent maturational levels which have been in the literature has demonstrated that the characterized by regional and developmental differences in functional properties [2,5,6,19,24,36,37]. The early postnatal develop ment of monoaminergic systems is well de fined; however, less is known about the role of these systems in the ontogenesis of certain behavioral patterns.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

1981

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Neonatal swimming behavior was studied after a single subcutaneous injection of L-dopa methyl ester (50 mg/kg; 200 mg/kg) apomorphine (0.1 mg/kg; 1.0. mg/kg), DL-amphetamine (0.5 mg/kg; 10 mg/kg), haloperidol (0.5 mg/kg; 1.0 mg/kg), L-tryptophan (50 mg/kg; 100 mg/kg), methysergide (1.0 mg/kg; 5.0 mg/kg) as well as intraventricular injection of 100 µg 6-OHDA. 1-, 3-, 5- and 7-day-old rats were placed into a temperature-controlled aquarium (37°C) and the pattern of motor coordination, latency time to swimming (LTS) and the number of foreleg strokes for 10 s (FS) were measured. When compared to the physiological saline-injected controls, rats that received L-dopa showed a striking increase of FS at all ages but the most striking improvement of motor coordination was found in newborn rats. On day 1 both doses of DL-amphetamine induced increases in FS and improvement of motor coordination, whereas apomorphine failed to show any effect at this age. On days 3, 5 and 7 low doses of DL-amphetamine and apomorphine increased the FS. However, high doses resulted in a decrement in swimming performance. Haloperidol impaired swimming on day 1 but produced a significant increase of FS on days 5 and 7. Neonatal injection of 6-OHDA delayed development of motor coordination, reduced FS and increased LTS. On days 3,5 and 7 high doses of L-tryptophan elicited an increase of FS, while high doses of methysergide caused significant impairment of performance. It is suggested that the brain rapidly converts the administered L-dopa to dopamine during the first week of life and there appears to be a strong dependent relationship between the pattern of motor coordination and the amount of available dopamine in the developing brain.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

1981

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“…As heparin has been shown to decrease tryptophan binding to albumin, serum was used for tryptophan measurement (9). Free and bound tryptophan were immediately separated by ultrafiltration (Amicon Centrifree ultrafilter) using fixed angle rotor centrifugation at room temperature for 20 min at 2000 X g. Total Trp concentrations in serum and free Trp in ultrafiltrates were measured immediately by an adaptation of an HPLC isocratic method with fluorometric detection as previously de-369 scribed (4,10).…”

Section: Methodsmentioning

confidence: 99%

Effect of Sodium Benzoate and Sodium Phenylacetate on Brain Serotonin Turnover in the Ornithine Transcarbamylase-Deficient Sparse-Fur Mouse

et al. 1988

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Herein we examine the effects of sodium benzoate and sodium phenylacetate on feeding and central serotonin turnover in a child with citrullinemia and in an animal model of congenital hyperammonemia, the ornithine transcarbamylase-deficient sparse-fur (spfly) mouse. In the child, when the benzoate/phenylacetate dosage was increased from 200 to 375 mg/kg/day each, feeding decreased. There was an accumulation of benzoate and phenylacetate in blood and cerebrospinal fluid a s well a s an increased concentration of 5-hydroxyindoleacetic acid, a neurochemical marker for serotonin turnover, in cerebrospinal fluid. In the mouse, sodium benzoate had a biphasic effect on both plasma ammonium levels and brain serotonin turnover. Two percent oral benzoate was associated with an increase in ammonium level, while a 3% dose led to a decrease in ammonium. There was a similar effect on serotonin turnover noted in both the hyperammonemic spfly and control CD-lly mice. Sodium phenylacetate did not have a consistent effect on serotonin turnover. The mechanism by which benzoate increases brain serotonin turnover appears to involve competition with tryptophan for albumin binding sites. This results in increased free tryptophan in serum and brain. W e speculate that some of the clinical symptoms of benzoate intoxication may be a consequence of altered serotonin turnover in the brain. We suggest that drug levels be monitored during therapy. 36excretion in children with inborn errors of urea synthesis (1). This has resulted in prolonged survival. However, both intravenous drugs used to treat acute hyperammonemia and inadvertent oral overdoses have been associated with clinical toxicity including anorexia, irritability, lethargy, and coma (1, 2). Symptoms of intoxication in part simulate those of hyperammonemia. The mechanism of these behavioral alterations is unclear. Bachmann et al. (3) re~orted increased brain uvtake of Tm. the precursor of serotbnin,tn rats injected with 1 mmol/kg of sddium benzoate. Increased brain uvtake of T m and increased brain serotonin turnover have also been reported in experimentally induced and naturally occurring hyperammonemia (4-7). These findings, together with data showing an association of anorexia with increased serotonin turnover in children with urea cycle disorders (8), suggest that benzoate intoxication may involve altered serotonin turnover.In studying the effect of benzoate and phenylacetate on serotonin turnover, we initially present a case report of a child with citrullinemia who developed toxic symptoms during high dose therapy and was found to have increased levels of the metabolite of serotonin, HIAA, in cerebrospinal fluid. We then examine in more detail the interaction of hyperammonemia and benzoate/ phenylacetate treatment on brain serotonin turnover in the chronically hyperammonemic ornithine transcarbamylase deficient sparse-fur (spf/y) mouse. METHODSBiochemical methods. Plasma ammonium was measured by a microfluorometric adaptation of a glutamate dehydrogenase method as previously d...

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“…Blood was collected into heparinized tubes with 25 iu heparin per ml of blood, a concentration which does not affect plasma Trp disposition (Bourgoin et al, 1974). The blood was then centrifuged and the resulting plasma separated into two portions.…”

Section: Plasma Metabolite Measurementsmentioning

confidence: 99%

“…This mechanism is largely involved during tryptamine (5-HT) depends on the concentration of ontogenesis (Bourgoin et al, 1974), food deprivation tryptophan (Trp), its precursor (Eccleston et al, 1965). (Knott & Curzon, 1972) or after immobilization Since tryptophan hydroxylase is normally un- (Knott & Curzon, 1972).…”

Section: Introductionmentioning

confidence: 99%

Effects of conditioned running on plasma, liver and brain tryptophan and on brain 5‐hydroxytryptamine metabolism of the rat

Chaouloff

Elghozi

Guezennec³

et al. 1985

British J Pharmacology

152

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1 An investigation was made into the effects of conditioned running (1 h and 2h at 20mmin-'), which accelerates lipolysis, on the concentrations of tryptophan (Trp) in plasma, liver and brain and on 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels in brain. 2 Running caused time-dependent increases in plasma free Trp and brain Trp of the rat, leading to increased brain 5-HT turnover as revealed by higher amounts of its metabolite, 5-HIAA. The ratio of brain Trp to plasma free Trp was decreased after 2 h of running. 3 Liver Trp content rose only after 3 h of running, while liver unesterified fatty acid (UFA) concentrations remained unmodified. 4 A comparison between food deprivation and running (both of which promote lipolysis) was performed. Running for 2 h affected to the same extent plasma Trp disposition when compared with 24 h food deprivation. Nevertheless, the ratio of brain Trp to plasma free Trp was decreased in the food-deprived rats, when compared to the runners. 5 Valine, an inhibitor ofentry ofTrp into the brain decreased its level there to the same extent in both controls and I h runners. 6 Nicotinic acid, which inhibits fat catabolism, completely abolished the plasma UFA increase induced by 1 h of running. The drug did not affect plasma free Trp, brain Trp, 5-HT or 5-HIAA but enhanced plasma total Trp level. 7 Naloxone, an opiate antagonist, which decreased running-induced lipolysis, did not alter plasma Trp disposition.8 Desipramine, an antidepressant compound, affected only peripheral Trp concentrations of the runners. Plasma free and total Trp concentrations were increased in desipramine-treated runners, compared with saline-treated runners. In addition, desipramine increased the ratio of brain Trp to plasma free Trp of the runners. Brain 5-HT and 5-HIAA were increased in both desipramine-treated controls and runners. 9 The results suggest that running, which like food deprivatiQn accelerates lipolysis, increases brain Trp content and then 5-HT turnover. Comparison of these two physiological situations suggests that effectiveness of brain Trp entry is much more altered by fasting.

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Plasma Tryptophan and 5‐ht Metabolism in the CNS of the Newborn Rat

Cited by 85 publications

References 25 publications

The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

Effect of Sodium Benzoate and Sodium Phenylacetate on Brain Serotonin Turnover in the Ornithine Transcarbamylase-Deficient Sparse-Fur Mouse

Effects of conditioned running on plasma, liver and brain tryptophan and on brain 5‐hydroxytryptamine metabolism of the rat

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