Perinatal Brain Serotonin Metabolism in Rats Malnourished in utero

Manjarrez-Gutiérrez, Gabriel; Chagoya, G.; Hernández, Jorge

doi:10.1159/000242857

Cited by 27 publications

(28 citation statements)

References 25 publications

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“…However, as we and others have shown, its effect on serotonergic metabolism in the brain appears to be more specific [5][6][7][8][9][10] . An essential amino acid, L -tryptophan (L-Trp), a protein constituent of the normal diet, is the precursor nutrient for the synthesis of brain serotonin (5-HT) [11,12] .…”

Section: Introductionmentioning

confidence: 48%

“…There is an acceleration of its biosynthesis as a consequence of a chronic increase of plasma free L-Trp entrance to the brain and in the activity of tryptophan hydroxylase [5][6][7][8][9][10][18][19][20] . The results reported here represent another important change in the serotonin metabolic path, and corroborate what our group previously reported.…”

Section: Discussionmentioning

confidence: 99%

“…These findings strongly suggest that it is neither the plasma concentration of albumin per se that determines the levels of unbound L-Trp nor the concentration of free fatty acids alone, but the poor binding of L-Trp to albumin which in IUGR infants favors its availability for 5-HT synthesis, which correlates well with the increased activity of TrpOH and acceleration of the neurotransmitter synthesis and function in the brain of IUGR rats [5][6][7][8][9]18] . Data from IUGR patients also show FFT elevated and brain 5-HT function increased, as have been observed in a dysfunction of brain sensory cortex [7,19,20] in the same type of patients.…”

Section: Discussionmentioning

confidence: 99%

“…Recent reported results show that in IUGR rats, there is an acceleration in brain 5-HT synthesis, starting in the fetal period and coincident with an elevation of FFT in plasma and brain and in the activity of tryptophan-5-hydroxylase 2 (TrpOH 2), which are associated to the serotoninergic neuronal system [6][7][8][9]18] . Infants with IUGR, also show an elevation of FFT in their plasma [7,19] , which suggests an increased transport of this precursor amino acid with enhancement of serotonin synthesis and activity in their brains [7,19,20] .…”

Section: Introductionmentioning

confidence: 99%

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Another Abnormal Trait in the Serotonin Metabolism Path in Intrauterine Growth-Restricted Infants

et al. 2008

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Background: The present study was aimed to obtain information on the interaction kinetics of L-tryptophan (L-Trp) with plasma albumin from normal, intrauterine growth-restricted (IUGR) and nutritionally recovered (NR) newborn infants. Methods: A case study cohort was planned in 37 newborns during the first 3 months of life. At birth two groups were formed. The first group included 20 newborns with IUGR. The control group (C) included 17 appropriate for gestational age newborns. At 30 days of age, 9 infants of the IUGR group showed a return to normal of the anthropometric parameters, these infants formed the NR group. Free, bound and total L-Trp were measured. To assess binding kinetics albumin was freed of fatty acids and tested in mole to mole samples from IUGR, NR and control babies. Results: Plasma free L-Trp was increased, K_d (dissociation constant) elevated and B_max(maximal binding)decreased in IUGR patients up to postnatal day 90. These changes remained even after nutritional recovery. Conclusions: Abnormal kinetics of L-Trp binding to albumin explains the increased availability of this precursor amino acid in the plasma of IUGR infants. This finding corroborates previous results in IUGR rats and newborn babies, indicating enhanced potential for brain serotonergic synthesis.

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Section: Introductionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Another Abnormal Trait in the Serotonin Metabolism Path in Intrauterine Growth-Restricted Infants

et al. 2008

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“…In light of the present findings of altered 5-HT turnover in IUGR, earlier contradictory reports might be explained in terms of different levels of stress to the fetus with IUGR. A low level of stress (IUGR of late onset) might induce a decreased 5-HT activity (43), and aggravated stress (IUGR of early onset) could produce increased activity (44). The latter might induce a precocious development of evoked potentials (12) due to an earlier switch from proliferation to differentiation (14).…”

Section: Discussionmentioning

confidence: 99%

Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia

Thordstein

Hedner

1992

Pediatr Res

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ABSTRACT. The effect of intrauterine growth retardation (IUGR) on cerebral and adrenal monoamine metabolism was studied in the fetuses of eight nulliparous rat dams after unilateral uterine artery ligation on d 18 of gestation.On d 22 (term = 23 d), four dams were subjected to normoxia and four to hypoxia (10% 0 2 ) for 58 min while their hemodynamics and blood gases were monitored. An inhibitor of L-aromatic-decarboxylase (3-hydroxybensylhydrazine) was infused to measure monoamine synthesis rate. After decapitation of the dam, fetuses were delivered by sectio, decapitated, and dissected at -5OC. The body, liver, forebrain, brainstem, and adrenal glands were weighed, and concentrations of monoamine precursors, transmitters, and metabolites were assessed in the three latter organs. The weights of liver and forebrain were reduced in fetuses with IUGR, whereas brainstem and adrenal weights were unaltered. Epinephrine content in adrenals was reduced in proportion to body weight under normoxia but failed to increase under hypoxia as it did in appropriately grown fetuses. There were only minor changes in monoamine metabolism in the brainstem. In the forebrain, however, marked changes were seen, mainly in serotonin metabolism: under normoxia, fetuses with IUGR had decreased levels of serotonin and its metabolite 5-hydroxyindole acetic acid. Under hypoxia, appropriately grown fetuses reduced their concentrations of these substances, whereas fetuses with IUGR paradoxically increased their synthetic activity. It is concluded that a disturbance of central nervous serotonin metabolism prevails in growth-retarded rat fetuses in late gestation and that this disturbance depends on the degree of growth retardation and the degree of perinatal stress. Fetuses and neonates who are small for gestational age because of IUGR are at increased risk to develop both minor (1, 2) and major (3, 4) neurodevelopmental sequelae. This could be due to an increased risk of asphyxia (5) or an increased sensitivity of the CNS in growth-retarded individuals (6). Indications of an altered central nervous function have been found in growthretarded human fetuses [motor function (7,8) and cardiovascular regulation (9)] and neonates [evoked potentials (lo)]. In growthretarded compared to AGA animal fetuses, changes of cerebral circulation (1 1) and evoked potentials (12) have been shown. Moreover, modifications of evoked potentials (6) and MA metabolism (13) are present in newborn growth-retarded animals when compared with AGA animals.Besides their role as neurotransmitters, MA have trophic effects on cerebral development (14), and manipulations of these systems perinatally have longstanding effects on cerebral function (15) and behavior (16,17). These transmitters, i.e. DA, NE, and 5-HT, have also been implied in the pathophysiology of brain damage from various kinds of stress (18)(19)(20). The growth-retarded fetus often suffers from a mild hypoxia (21) and an insufficient supply of essential amino acids (22), which could influence the synthesis of th...

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Chronicity in anorexia nervosa: Pregnancy and birth complications as risk factors

Bakan

Birmingham

Goldner

1991

Int. J. Eat. Disord.

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The chronic form of anorexia nervosa (AN) affects about one‐quarter of patients and has serious somatic and psychological consequences. This paper presents evidence in support of the hypothesis that pregnancy and birth complications (PBCs) associated with neuropathology may be risk factors for chronic anorexia nervosa. There is increasing evidence that PBCs are risk factors for other psychiatric and somatic disorders. Recent findings of possible premorbid neuropathology in patients with anorexia nervosa suggest that PBCs may be risk factors for chronicity in anorexia nervosa. Topics discussed include the origins of constitutional vulnerability to anorexia nervosa, correlates of PBCs and of chronic anorexia nervosa, the relationship of PBCs to neurological and neurochemical abnormalities, chronicity of anorexia nervosa in relation to PBCs and to neurological and neurochemical abnormalities, and the research implications of the hypothesis that PBCs and associated neuropathology are risk factors for chronicity in anorexia nervosa.

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Perinatal Brain Serotonin Metabolism in Rats Malnourished in utero

Cited by 27 publications

References 25 publications

Another Abnormal Trait in the Serotonin Metabolism Path in Intrauterine Growth-Restricted Infants

Another Abnormal Trait in the Serotonin Metabolism Path in Intrauterine Growth-Restricted Infants

Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia

Chronicity in anorexia nervosa: Pregnancy and birth complications as risk factors

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