Effect of Neonatal Thyroid Deficiency on the Catecholamine, Substance P, and Thyrotropin-Releasing Hormone Contents of Discrete Rat Brain Nuclei

Dupont, André; Dussault, J H; Rouleau, Dominique M.; Paolo, Thérèse Di; Coulombe, Pierre A.; Gagné, Bernard; Mérand, Yves; Moore, Stanley A.; Barden, Nicholas

doi:10.1210/endo-108-6-2039

Cited by 44 publications

(15 citation statements)

References 40 publications

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“…Singhal et al (30) reported increased levels of 5-HIAA associated with lowered 5-HT concentrations. More recently, Dupont et al (31) found no significant changes in the hypothalamic concentration of either DA or NE in hypothyroid rats, but catecholamine metabolite concentrations awere not examined in that study.…”

Section: Discussionmentioning

confidence: 67%

Serotoninergic Control of Growth Hormone Secretion: Hypothalamic Dopamine, Norepinephrine, and Serotonin Levels and Metabolism in Three Hyposomatotropic Rat Models and in Normal Rats*

et al. 1982

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The relationship between the activity of the brain biogenic monoamines dopamine (DA), norepinephrine (NE), and serotonin (5-HT) and pituitary GH release remains controversial due to the previous use of indirect and nonspecific techniques. The aim of this investigation was to determine directly and specifically the relative activities (turnover) of hypothalamic DA, NE, and 5-HT in rat models of pituitary GH deficiency and GH hypo-or hypersecretion. These models were 1) adult rats after neonatal monosodium-L-glutamate (MSG) treatment, 2) hypophysectomized rats with and without GH replacement, 3) hypothyroid [propylthiouracil (PTU)-treated] rats, and 4) normal rats. Selected ion monitoring (computerized gas chromatography-mass spectrometry) was used to specifically and simultaneously assay hypothalamic concentrations of DA, NE, and 5-HT and their major metabolites. The turnover or activity of each amine in the hypothalami was estimated from the ratio of metabolite to amine in each case as well as by the use of the monoamine oxidase inhibitor pargyline for MSG-treated rats.In MSG-treated rats, there was a marked reduction (P < 0.0025) in the hypothalamic turnover of 5-HT which was associated with a significant fall (P < 0.05) in serum GH concentrations. In hypox rats, there was found to be a highly significant increase (P < 0.01) in hypothalamic 5-HT turnover, which was corrected to control levels after a course of GH treatment. In the hypothyroid rats, there was also a highly significant increase in the hypothalamic ratio of 5-hydroxyindoleacetic acid to 5-HT within 6 days of commencing PTU treatment, and this ratio remained elevated (P < 0.0025) after 38 days PTU uptake. This increased 5-HT activity was associated with a significant increase in GH secretion (P < 0.01; by 6 days), but after 38 days on PTU, when pituitary GH was depleted, serum levels were significantly less (P < 0.05) than controls. In the group of normal rats, 10 of 44 of the animals exhibited very high GH concentrations (>250 ng/ml). The mean hypothalamic 5-hydroxyindoleacetic acid to 5-HT ratio in these animals was highly significantly greater (P < 0.0005) than that in the remaining 34 animals, all of which had serum GH levels below 90 ng/ml. We propose that the high 5-HT turnover and high serum GH concentrations are directly related. There was no relationship between turnover or concentrations of DA or NE and GH status in these studies.The conclusions from this investigation are that hypothalamic 5-HT activity is directly related to GH secretory status in the rat and that serotoninergic pathways participate in GH negative feedback effects in the hypothalamus. (Endocrinology 110: 376, 1982) T HE ROLES of specific monoamine neuronal pathways in the central stimulation of GH release have yet to be convincingly elucidated. The case of central control of GH is a particularly confusing one, and in a recent review, Krulich (1) cited considerable evidence favoring a role for all three major brain monoamines, dopamine (DA), norepinephrine (NE), and s...

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Section: Discussionmentioning

confidence: 67%

Serotoninergic Control of Growth Hormone Secretion: Hypothalamic Dopamine, Norepinephrine, and Serotonin Levels and Metabolism in Three Hyposomatotropic Rat Models and in Normal Rats*

et al. 1982

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“…The expression of the NGFI-A gene, an immediate-early response gene implicated in the control of brain cell proliferation and aspects of brain development, is directly regulated by T3 in the brain of the neonatal, but not the adult, rat (Pipaon et al, 1992). Furthermore, animal studies suggest that manipulations of thyroid hormone status can have profound effects on catecholamine neurotransmitter systems in both the neonatal and the adult rat brain (Rastogi and Singhal, 1979;Dupont et al, 1981 ). These studies are of particular importance, as alterations of catecholamine neurotransmitter systems have been implicated in the pathogenesis of ADHD (Shenker, 1993).…”

Section: Thyroid Hormone and Normal Neurodevelopmentmentioning

confidence: 99%

Resistance To Thyroid Hormone: Implications for Neurodevelopmental Research On the Effects of Thyroid Hormone Disruptors

1998

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Thyroid hormones are essential for normal behavioral, intellectual, and neurological development. Congenital hypothyroidism, if not treated, can result in irreversible mental retardation, whereas thyroid diseases with more moderate impairment of thyroid function, such as resistance to thyroid hormone, cause less severe intellectual and behavioral abnormalities, including attention deficit hyperactivity disorder. There is increasing evidence that exposure to certain synthetic compounds, including dioxins and polychlorinated biphenyls (PCBs), during the perinatal period can also impair learning, memory, and attentional processes in offspring. Animal and human studies suggest that exposure to these environmental toxicants impair normal thyroid function. Although the precise mechanisms of action of the adverse effects these toxicants have on neurodevelopment have not yet been elucidated, it is possible that they are partially or predominantly mediated by alterations in hormone binding to the thyroid hormone receptor. The convergence of studies that examine the neurodevelopmental consequences of moderate impairment of thyroid function, such as is found in resistance to thyroid hormone, with those studies that demonstrate the adverse behavioral and cognitive effects of perinatal exposure to dioxins and PCBs serves to generate new hypotheses to test in a research setting. Such studies may provide new insights into the basic pathogenesis of developmental neurotoxicity following exposure to thyroid-disrupting synthetic compounds.

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“…The central regulation of thyroid hormone secretion by monoam i ne neurotr ansm itters through the by poth a l am i c-p i to i tary pathway has been documented by many Investigators (32)(33)(34)(35). It is generally accepted that dopamine and serotonin have antagonistic effects (36).…”

Section: Hypothalamic-pituitary-thyroid Axismentioning

confidence: 99%

Neurobiology of Pyridoxine

Dakshinamurti

1982

Advances in Nutritional Research

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Pyridoxal 5'-phosphate (PLP) is the major coenzymatic form of pyridoxine. There are over one hundred known pyridoxal 5'-phosphate-dependent reactions, most of which are involved in the metabolism of various amino acids . Pyridoxamine 5'-phosphate can function in aminotransf erase reactions by the cyclic regeneration of the two active phosphate forms. Pyridoxal 5'-phosphate-dependent reactions studied in the nervous system are involved in the catabolism of various amino acids.The putative neurotransmitters , dopamine, norepinephrine , serotonin , histamine , aminobutyric acid and taurine , as well as the sphingoiipids and poly amines are synthesized by PLP-dependent enzymes. Of these enzymes, three ( glutamic acid decarboxylase , 5-hydroxytryptophan decarboxylase and crnithine decarboxylase) seem to have crucial roles (Fig. '). The clinical effects of pyridoxine deficiency can be explained on the basis of the known decreases in the activities of these enzymes (1). EXPERIMENTAL PYRIDOXINE DEFICIENCY IN THE NEONATE RATDakshinamurti and Stephens ( 2) first reported the production of congenital pyridoxine deficiency .Our observations extended the "chronic fetal distress" hypothesis of Gruenwald ( 3) to include effects on the development of the central nervous system. We later showed that a deficiency of pyridoxine in rat pups could be produced by depriving the dam of dietary pyridoxine during lactation (4). Such a deficiency has been characterized using biochemical and electrophysiological parameters. The electroencephalogram (EEG)

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Effect of Neonatal Thyroid Deficiency on the Catecholamine, Substance P, and Thyrotropin-Releasing Hormone Contents of Discrete Rat Brain Nuclei

Cited by 44 publications

References 40 publications

Serotoninergic Control of Growth Hormone Secretion: Hypothalamic Dopamine, Norepinephrine, and Serotonin Levels and Metabolism in Three Hyposomatotropic Rat Models and in Normal Rats*

Serotoninergic Control of Growth Hormone Secretion: Hypothalamic Dopamine, Norepinephrine, and Serotonin Levels and Metabolism in Three Hyposomatotropic Rat Models and in Normal Rats*

Resistance To Thyroid Hormone: Implications for Neurodevelopmental Research On the Effects of Thyroid Hormone Disruptors

Neurobiology of Pyridoxine

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