Effects of p-chlorophenylalanine on time of neuronal origin during embryo-genesis in the rat

Lauder, Jean M.; Krebs, Helmut

doi:10.1016/0006-8993(76)90153-0

Cited by 123 publications

(37 citation statements)

References 35 publications

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“…In AGA fetuses under hypoxia, the concentrations of 5-HT and 5-HIAA were both reduced compared to those under normoxia, whereas, surprisingly, fetuses with IUGR demonstrated a marked increase in synthetic activity compared to AGA fetuses. The background to this paradoxical reaction might be related to changes in the activity of excitatory amino acid transmitters (4 1, 42) or to increased levels of maternal or fetal glucocorticoids (14). 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.…”

Section: Discussioncontrasting

confidence: 42%

“…This could be the result of later-developing parts being more sensitive to adverse influences or an active process favoring the most important parts where centers for autonomic control are located. Because 5-HT has been shown to have trophic effects on brain development and metabolism (14,46), the present findings of a reduced 5-HT activity under basal conditions could, if extrapolated to the human situation, be part of the pathophysiology of retarded forebrain development, motor function in fetuses (7,8,40), and evoked potentials in neonates (10).…”

Section: Discussionmentioning

confidence: 99%

“…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%

“…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.…”

mentioning

confidence: 99%

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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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Section: Discussioncontrasting

confidence: 42%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Thordstein

Hedner

1992

Pediatr Res

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“…Experimental evidence indicates that serotonin can influence embryogenesis and growth (3,4) presumably by acting as a developmental signal (5) or as a neurotrophic factor as well (6). Furthermore, serotonin seems to play a role in regulating the development of the mammalian brain through its action on the production of self serotonin neurons (4,7,8) and on target tis-sues innervated by serotoninergic neurons (9)(10)(11). Pharmacological or nutritional manipulations during pregnancy or the suckling period can induce drastic morphological and functional changes in the growth and development of the nervous system (12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Neonatal administration of citalopram delays somatic maturation in rats

Deiró

Manhães-de-Castro

Cabral-Filho³

et al. 2004

Braz J Med Biol Res

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We investigated the somatic maturation of neonate rats treated during the suckling period with citalopram, a selective serotonin reuptake inhibitor. Groups with 6 male neonates were randomly assigned to different treatments 24 h after birth. Each litter was suckled by one of the dams until the 21st postnatal day. Body weight, head axis and tail length were measured daily from the 1st to the 21st postnatal day. Time of ear unfolding, auditory conduit opening, incisor eruption, and eye opening was determined. Pups received 5 mg (Cit5), 10 mg (Cit10) or 20 mg/kg (Cit20) citalopram sc, or saline (0.9% NaCl, w/v, sc). Compared to saline, body weight was lower (24.04%, P < 0.01) for Cit10 from the 10th to the 21st day and for Cit20 from the 6th to the 21st day (38.19%, P < 0.01). Tail length was reduced in the Cit20 group (15.48%, P < 0.001) from the 8th to the 21st day. A reduction in mediolateral head axis (10.53%, P < 0.05) was observed from the 11th to the 21st day in Cit10 and from the 6th to the 21st day in Cit20 (13.16%, P < 0.001). A reduction in anteroposterior head axis was also observed in the Cit20 group (5.28%, P < 0.05) from the 13th to the 21st day. Conversely, this axis showed accelerated growth from the 12th to the 21st day in the Cit5 group (13.05%, P < 0.05). Auditory conduit opening was delayed in the Cit5 and Cit20 groups and incisor eruption was delayed in all citalopram groups. These findings show that citalopram injected during suckling to rats induces body alterations and suggest that the activity of the serotoninergic system participates in growth mechanisms.

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Distribution and changes in ?- and ?-opiate receptors during the midlife neurodevelopmental period of coho salmon,Oncorhynchus kisutch

1996

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Parr-smolt transformation (PST) in coho salmon is associated with a plasma thyroid hormone (PT4) surge and a critical period of neural development that includes axonal sprouting, neurogenesis, and surges of select neurotransmitters. Here we provide a description of the selectivity, distribution, and the changes in the density of mu- and kappa-opiate receptors during PST, as revealed by quantitative in vitro autoradiography of [3H]Tyr-D-Ala-Gly-NMe-Phe-Gly-ol ([3H]DAMGO) and [3H]ethylketocyclazocine ([3H]EKC), respectively. The concentration of mu-receptors increased significantly in select cell groups in the early stages of parr-smolt transformation, until a peak was reached at the time coinciding with the peak of the PT4 surge. In other cell groups, the peaks occurred 1 or 2 weeks later. With one exception, this increase was followed by a decrease in concentration. The brain areas showing the highest concentrations are the dorsal nucleus of the ventral telencephalic area, the glomerular region, the granular layer of the valvula cerebelli, the nucleus diffuses of the inferior lobe, and the nucleus diffuses of the torus lateralis. Other regions with distinctly elevated mu-receptor concentrations are the stratum griseum centrale of the optic tectum and the preoptic area. The distribution of kappa-receptors is more diffuse, and the densities are considerably lower. The overlap in distribution of mu- and kappa-receptors is considerable, but significant exceptions are noted. For example, the dorsomedial nucleus of the dorsal telencephalic area, the habenular nucleus, and the dorsomedial nucleus of the thalamus exhibit a surge in density of kappa-receptors at the time of the PT4 surge, while the density of mu-receptors in these nuclei remain very low throughout parr-smolt transformation. The kappa-receptor containing cell groups are not identifiable until 3 weeks before the PT4 surge because of low densities. The most prominently labeled kappa-receptor regions are the ventral and dorsal nuclei of the ventral telencephalic area, the medial and dorsal zones of the dorsal telencephalic area, the optic tectum (all layers), the dorsomedial nucleus of the thalamus, the torus lateralis of the ventral hypothalamus, and the preoptic area. An increase of mu- and kappa-opiate receptor densities in specific brain regions may reflect roles in the alteration of brain organization, olfactory imprinting, neuroendocrine activity or other physiological activities. The overall distribution of these receptors are relatively more extensive in salmon than in other vertebrates so far studied.

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Effects of p-chlorophenylalanine on time of neuronal origin during embryo-genesis in the rat

Cited by 123 publications

References 35 publications

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

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

Neonatal administration of citalopram delays somatic maturation in rats

Distribution and changes in ?- and ?-opiate receptors during the midlife neurodevelopmental period of coho salmon,Oncorhynchus kisutch

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