Prenatal ontogenesis ofp-,m-octopamine and phenylethanolamine in relation to catecholamines and their metabolizing enzymes in the developing rat brain and heart

David, Jean‐Claude; Cavoy, Albert; Coulon, J.F.; Delacour, Jean

doi:10.1016/0306-4522(84)90020-4

Cited by 8 publications

(6 citation statements)

References 27 publications

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“…A decade ago, Saavedra et al (1974) found that there are peaks of OA and phenylethanolamine (PeOH) contents in the embryonic rat brain before the appearance of significant monoamine oxidase (MAO) activity. This observation of the OA change has been extended recently by David et al (1983) by separation of the two isomers. The peak of OA is limited to the para isomer and to the brain tissue, a continuous increase being observed in the developing heart.…”

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confidence: 67%

“…Since 1974, this observation has not yet led to an understanding of the possible physiological functions of OA and related phenolamines in mammals. However, recent progress in the determination and accurate separation of these amines (Danielson et al, 1977;David, 1977) has made it possible to suggest that p-OA has a neuromodulator role in neurovegetative processes (David and Delacour, 1980;David et al, 1983;Delacour et al, 1983). The close relationship between OA and genetic or acquired behavior (David and Delacour, 1980) suggested developmental neurochemical investigations.…”

Section: Discussionmentioning

confidence: 99%

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Relationship Between Phenolamines and Catecholamines During Rat Brain Embryonic Development In Vivo and In Vitro

David

1984

Journal of Neurochemistry

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p-Octopamine and phenylethanolamine are present in the embryonic rat brain earlier than catecholamines. These phenolamines are localized mainly in the hypothalamus, where the level of p-octopamine is very high. The parallel developmental study of the activities of dopamine beta-hydroxylase, 3,4-dihydroxyphenylalanine decarboxylase, tyrosine hydroxylase, and monoamine oxidase shows that phenolamines are present in significant amounts in the hypothalamus until tyrosine hydroxylase and monoamine oxidase become catalytically active. The culture of embryonic hypothalamus at different ages shows that no tyrosine hydroxylase and monoamine oxidase activities can be detected if the tissue is cultured before 15 days. This clearly indicates that all the enzymes related to catecholamine biosynthesis are not triggered at the same time during the development of the rat brain. These results are discussed on the basis of the physiological importance of phenolamines in mammals and of the use of the developing rat brain as a model for the study of the onset of the catecholaminergic system and the decline of the octopamine.

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confidence: 67%

Section: Discussionmentioning

confidence: 99%

Relationship Between Phenolamines and Catecholamines During Rat Brain Embryonic Development In Vivo and In Vitro

David

1984

Journal of Neurochemistry

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“…Noncatecholic amines (i.e., phenolamines) have been observed at early stages of fetal rat brain development (Saavedra et al, 1974). More recently this oc-currence has been found to be localized to the hypothalamus and to precede that of catecholamines (David, 1984;David et al, 1984). Some of the biosynthetic pathways for phenolamines are similar to the steps of catecholamine production (Boulton, 1976;Robertson and Juorio, 1976;Robertson, 198 1; David and Coulon, 1985).…”

Section: Discussionmentioning

confidence: 96%

“…Among the enzymes involved in the biosynthesis of catecholamines, TH is specific for the catecholamine pathway and is the rate-limiting step (Nagatsu, 1964). The others, like aromatic L-amino-acid decarboxylase (AADC) and DBH, are more ubiquitous and are also involved in the biosynthesis of phenolamines (Brandau and Axelrod, 1972;David, 1984;David et al, 1984). During development of rat brain, the two phenolamine and catecholamine pathways appear to be sequentially represented, first phenolamine from 13 to 15 days and catecholamine after 14.5 days (Coyle and Henry, 1973).…”

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confidence: 99%

Gene Expression of Tyrosine Hydroxylase in the Developing Fetal Brain

Coulon

Biguet

Cavoy

et al. 1990

Journal of Neurochemistry

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Tyrosine hydroxylase, aromatic L-amino-acid decarboxylase, and dopamine beta-hydroxylase activities were studied in the developing fetal rat brain. A delay of 2-3 days between the detection of the tyrosine hydroxylase and the aromatic L-amino-acid decarboxylase and dopamine beta-hydroxylase activities was observed. For this reason, the expression of tyrosine hydroxylase mRNA was studied. Tyrosine hydroxylase mRNA was visualized in the whole brain from 13 days of gestation, but the largest increase of the expression was observed in the hypothalamus. These results are discussed in terms of the relative gene expressions of the three enzymes involved in the biosynthesis of catecholamines and phenolamines in nervous tissues.

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“…Both NE and E were detectable in the heart on day e17, one day after a 5-fold increase in dopa decarboxylase, which converts L-DOPA to dopamine, the substrate for NE synthesis. Cardiac NE and E at day e17 probably do not come from L-DOPA synthesized in the heart, since tyrosine hydroxylase was undetectable in the heart at e17 and is ®rst detectable at day e18 [6]. Even at birth tyrosine hydroxylase containing nerve ®bers are rare in rat heart [17,21,25] as most cardiac sympathetic innervation develops postnatally [2,22].…”

Section: Discussionmentioning

confidence: 99%

Ontogeny of epinephrine metabolic pathways in the rat: role of glucocorticoids

Kennedy

2000

Intl J of Devlp Neuroscience

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Recent studies suggest that the initial expression of adrenal phenylethanolamine N-methyltransferase (PNMT) and epinephrine (E) are dependent upon stimulation of adrenal glucocorticoid receptors. However, evidence suggests that the expression of heart and brain PNMT is independent of glucocorticoids. We measured PNMT activity and E levels in adrenal, heart and head over the latter half of gestation in rat fetuses treated chronically with glucocorticoids, and in normal controls. Chronic glucocorticoid treatment ending on embryonic day (e)12 did not affect heart, head or trunk PNMT activity or E levels. In contrast, chronic glucocorticoid exposure ending e19 or e20 resulted in marked increases in both PNMT and E in adrenal, heart and head tissues. The elevation of E in all three tissues was unaffected by maternal adrenalectomy, indicating enhanced fetal E synthesis. In the absence of exogenous glucocorticoid treatment heart PNMT activity peaked on e12, prior to the earliest reported appearance of glucocorticoid receptors. We conclude that expression of PNMT in all three tissues is glucocorticoid independent until the latter part of gestation when it is readily enhanced by glucocorticoids.

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Prenatal ontogenesis ofp-,m-octopamine and phenylethanolamine in relation to catecholamines and their metabolizing enzymes in the developing rat brain and heart

Cited by 8 publications

References 27 publications

Relationship Between Phenolamines and Catecholamines During Rat Brain Embryonic Development In Vivo and In Vitro

Relationship Between Phenolamines and Catecholamines During Rat Brain Embryonic Development In Vivo and In Vitro

Gene Expression of Tyrosine Hydroxylase in the Developing Fetal Brain

Ontogeny of epinephrine metabolic pathways in the rat: role of glucocorticoids

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