Daily variations of various parameters of serotonin metabolism in the rat brain. II. Circadian variations in serum and cerebral tryptophan levels: Lack of correlation with 5-HT turnover

Héry, F.; Chouvet, Guy; Kan, Jean-Paul; Pujol, Jean‐François; Głowiński, J.

doi:10.1016/0006-8993(77)90648-5

Cited by 62 publications

(15 citation statements)

References 24 publications

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“…Noteably, the qualitatively different response between the two treatments indicates that, in contrast to the cortex, where TTX suppressed the effect of tryptophan loading [45], the onset of the 5-HIAA peak in the SCN may not be triggered by tryptophan in take. Consistent with this idea is that the evening rise in 5-HIAA in the present study occurred before lights-off, when the hamsters are asleep, and that circadian variation in blood and brain tryptophan levels are not correlated with serotonin turnover [38].…”

Section: Discussionsupporting

confidence: 81%

“…The disruptive effects of lesions of the raphe nuclei or their projections [12][13][14] and pharmacological manipulations of serotonin synthesis and degradation [15][16][17][18][19][20] on behavioral and endocrine rhythms underscore the importance of serotonin. Although the basis for the action ofserotonin in the SCN has not yet been established, diurnal rhythms in hypothalamic serotonin concentration [25,38,39], uptake [23,24] and electrophysiological effects [4,21,40] have been observed. Moreover, striking diurnal fluctuations in the extracellular concentra tion of the principal serotonin metabolite, 5-HIAA, have been documented in the mammalian SCN [26,27], Collec tively, these results give strong evidence that modulation of responsiveness of serotonin targets in the SCN together Time, min with regulated timing of serotonin release are important to the regulation of pacemakerfunction.…”

Section: Discussionmentioning

confidence: 99%

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Diurnal Variation in 5-Hydroxyindole-Acetic Acid Output in the Suprachiasmatic Region of the Siberian Hamster Assessed by in vivo Microdialysis: Evidence for Nocturnal Activation of Serotonin Release

Ww²,

Sa³

et al. 1992

Neuroendocrinology

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In vivo brain microdialysis was used to characterize the daily pattern of 5-hydroxyindole-acetic acid (5-HIAA) release in the region of the suprachiasmatic nuclei (SCN) in freely behaving male Siberian hamsters housed under 16L:8D. A marked diurnal variation in the concentration of extracellular 5-HIAA was apparent, with peak levels (147 ± 5% of the daily mean; p < 0.05) occurring 2-3 h after lights-off. Smaller nocturnal rises in extracellular 5-HIAA were observed in the posterior hypothalamus and preoptic area (128 ± 4 and 123 ± 8% of the daily mean, respectively; both p < 0.05 vs. average daytime levels). Tryptophan loading increased 5-HIAA in SCN microdialysates by 44 ± 6%, and this response was enhanced by localized perfusion with tetrodotoxin (TTX; 5 µM). Localized applications of KC1 (150 mil) or veratridine (100 µM) decreased 5-HIAA by 62 ± 5 or 49 ± 11%, respectively. The effect of KC1 was not significantly affected by specific calcium channel blockers. Perfusion with TTX markedly decreased SCN 5-HIAA during the dark phase, but had little effect during the light phase (42 ± 8 vs. 12 ± 5% suppression, respectively; p < 0.01). Addition of serotonin (3 µM) to the perfusate significantly stimulated 5-HIAA output. This treatment increased the release of 5-HIAA more during the dark than during the light phase (61 ± 8 vs. 25 ± 5%, respectively; p < 0.01). Taken together, these results are evidence that: (1) there is increased TTX-sensitive (synaptic) release of serotonin at night that could contribute to the nocturnal rise in the extracellular concentration of 5-HIAA in the SCN; (2) clearance (uptake and/or metabolism) of extracellular serotonin in the SCN is higher at night; (3) 5-HIAA release in the SCN of the Siberian hamster is similar to that reported for other areas of the brain in other species, and (4) variations in 5-HIAA may, under certain physiological conditions, reflect changes in the extracellular concentration of serotonin.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Diurnal Variation in 5-Hydroxyindole-Acetic Acid Output in the Suprachiasmatic Region of the Siberian Hamster Assessed by in vivo Microdialysis: Evidence for Nocturnal Activation of Serotonin Release

Ww²,

Sa³

et al. 1992

Neuroendocrinology

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“…dilution of this "tryptophan-free" medium with fresh (truly tryptophan-free) medium. Adding exogenous tryptophan to the medium at concentrations within the range others have measured in cerebrospinal fluid of untreated rats (1-3 p M ) (Sarna et al, 1983;Hutson et al, 1985;Anderson et al, 1987) caused elevations in tissue tryptophan levels quantitatively similar to those which occur physiologically in rat brain, e.g., with exercise (Chaouloff et al, 1985(Chaouloff et al, , 1986, certain stressors (Knott et al, 1973;Kennett and Joseph, 1981;Culman et al, 1984;Dunn, 1988), ingestion of a carbohydrate-rich meal (Fernstrom and Wurtman, 1971 b;Colmenares et al, I975), or diurnal variation (Morgan et al, 1975;Hery et al, 1977).…”

Section: Discussionmentioning

confidence: 93%

Tryptophan Availability Modulates Serotonin Release from Rat Hypothalamic Slices

Schaechter

Wurtman

1989

Journal of Neurochemistry

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Application of a novel in vitro experimental system has allowed us to describe the relationship between tryptophan availability and serotonin release from rat hypothalamic slices. Superfusing hypothalamic slices with a physiologic medium containing /-tryptophan ( 1, 2, 5 , or 10 p M ) caused dose-dependent elevations in tissue tryptophan levels; the magnitude of the elevations produced by supplementing the medium with <5 pM tryptophan was within the physiologic range for rat brain tryptophan levels. Slice serotonin levels rose biphasically as the tryptophan concentration in the medium was increased. Superfusing the slices with medium supplemented with a low tryptophan concentration (1 or 2 p M ) caused proportionally greater incremental changes in serotonin levels than the increases caused by further elevating the tryptophan concentration ( 5 or 10 p M ) . The spontaneous release of serotonin from the slices exhibited a dose-dependent relationship with the tryptophan concentration of the superfusion medium, Electrically evoked serotonin release, which was calcium-dependent and tetrodotoxin-sensitive, also increased in proportion to the medium tryptophan concentration. These data suggest that the rate at which serotonin is released from hypothalamic nerve terminals is coupled to brain tryptophan levels. Accelerations in hypothalamic serotonin synthesis, caused by elevating brain tryptophan levels, result in proportionate increases in the rates of serotonin release during rest and with membrane depolarization. Key Words: Serotonin release-Tryptophan availability-Hypothalamus-Superfused brain slices. Schaechter J. D. and Wurtman R. J. Tryptophan availability modulates serotonin release from rat hypothalamic slices. J. Neurochem. 53, 1925-1933 (1989).The rate at which the brain synthesizes serotonin (5-HT) in vivo varies with its tryptophan concentration (Eccleston et al., 1965; Weber and Horita, 1965;Moir and Eccleston, 1968). This relationship exists because the rate-limiting enzyme in 5-HT biosynthesis, tryptophan hydroxylase, is unsaturated with tryptophan. The concentration of tryptophan normally present in the brain (approximately 10-40 p M ) (Curzon, 1986) is less than the estimated K,,, of tryptophan hydroxylase for its amino acid substrate (50 p M ) (Friedman et al., 1972), and thus much less than that needed for full saturation of the enzyme. Hence, treatments which raise brain tryptophan levels within their physiologic range (e.g

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“…Under normal circumstances, the concentration of tryptophan metabolites of this pathway are between 100-and 1000-fold lower than the concentration of tryptophan in the brain [Saito et al, 1993]. In comparison, the sum of the concentrations of serotonin and its metabolite 5-HIAA is approximately one-fifth the concentration of tryptophan in brain [Hery et al, 1977]. Therefore, the kynurenine pathways are not expected to contribute significantly to the accumulation of AMT in brain under normal circumstances.…”

Section: Evidence For Role Of Serotonin In Epilepsymentioning

confidence: 96%

Serotonin in autism and pediatric epilepsies

Chugani

2004

Ment. Retard. Dev. Disabil. Res. Rev.

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Serotonergic abnormalities have been reported in both autism and epilepsy. This association may provide insights into underlying mechanisms of these disorders because serotonin plays an important neurotrophic role during brain development-and there is evidence for abnormal cortical development in both autism and some forms of epilepsy. This review explores the hypothesis that an early disturbance in the serotonin system affects cortical development and the development of thalamocortical innervation, and is a potential mechanism, common to autism and pediatric epilepsies associated with cortical dysplasia. An argument is made that cortical malformation leads to abnormalities of thalamocortical connectivity, and that serotonin plays a critical role in this process. Finally, a role for altered metabolism of the serotonin precursur, tryptophan, in both epilepsy and autism is discussed. Key Words: serotonin; autism; epilepsy; tryptophan; cortical development; kynurenine E pilepsy is more common among autistic children than in the general population; conversely, autism (or milder pervasive developmental disorders) is more common in epileptic children than in the general population. There is evidence for abnormalities of the neurotransmitter serotonin in both epilepsy and autism. The role of serotonin in brain development is briefly reviewed here and then the evidence considered for a role of an altered serotonin system in these developmental disorders. We hypothesize that serotonergic abnormalities during prenatal and early postnatal development may lead to changes in thalamocortical connectivity, which results in a predisposition for autism and epilepsy. In addition, we discuss the involvement of aberrant metabolism of tryptophan-the metabolic precursor of serotonin-as a potential mechanism for alterations in serotonin availability.

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Daily variations of various parameters of serotonin metabolism in the rat brain. II. Circadian variations in serum and cerebral tryptophan levels: Lack of correlation with 5-HT turnover

Cited by 62 publications

References 24 publications

Diurnal Variation in 5-Hydroxyindole-Acetic Acid Output in the Suprachiasmatic Region of the Siberian Hamster Assessed by in vivo Microdialysis: Evidence for Nocturnal Activation of Serotonin Release

Diurnal Variation in 5-Hydroxyindole-Acetic Acid Output in the Suprachiasmatic Region of the Siberian Hamster Assessed by in vivo Microdialysis: Evidence for Nocturnal Activation of Serotonin Release

Tryptophan Availability Modulates Serotonin Release from Rat Hypothalamic Slices

Serotonin in autism and pediatric epilepsies

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