Serotonin, 5-hydroxyindoleacetic acid and substance P content of discrete brain nuclei in rats made hypo- or hyperthyroid in the neonatal period: Effect of growth hormone treatment

Savard, Pierre; Blanchard, Louise M.; Mérand, Yves; Dupont, André

doi:10.1016/0165-3806(84)90101-9

Cited by 6 publications

(6 citation statements)

References 34 publications

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“…However, comorbidity of depression and hyperthyroidism does not sustain the hypothesis of serotoninergic deficiency (Bahls and de Carvalho, 2004). Also, Savard et al (1984) observed that neonatal hyperthyroidism induced very little modification of 5‐HT, 5‐hydroxyindoleacetic acid (5‐HIAA) and substance P concentrations in discrete nuclei of the rat brain. Further neuroendocrine studies are needed to assess subtypes of 5‐HT receptors aiming to confirm and explain more specifically the pathophysiological condition of serotonin in thyroid alterations.…”

Section: Thyroid Hormones and Neurotransmitters Interactionsmentioning

confidence: 99%

“…Severe hypothyroxinemia has been associated with increased morbidity and long‐term disability in premature infants (Den Ouden et al, 1996; Reuss et al, 1996). The abnormal brain development observed during hypothyroidism may, in part, result from absence of growth hormone (Savard et al, 1984). On other hand, there are three types or combinations of thyroid deficiency states known to impact fetal development (Xue‐Yi et al, 1994; Glinoer, 1997; Oppenheimer and Schwartz, 1997; Haddow et al, 1999): (1) isolated maternal hypothyroidism; (2) isolated fetal hypothyroidism (sporadic congenital hypothyroidism); and (3) iodine deficiency‐combined maternal and fetal hypothyroidism.…”

Section: Thyroid Hormones and Fetal Brain Developmentmentioning

confidence: 99%

See 1 more Smart Citation

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

279

254

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The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.

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Section: Thyroid Hormones and Neurotransmitters Interactionsmentioning

confidence: 99%

Section: Thyroid Hormones and Fetal Brain Developmentmentioning

confidence: 99%

Thyroid hormones states and brain development interactions

Ahmed

El-Gareib

El-Bakry

et al. 2007

Intl J of Devlp Neuroscience

279

254

View full text Add to dashboard Cite

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“…A reduction in 5-HT turnover in the MBH of GHinjected birds was indicated, however, by the reduc¬ tion in 5-HIAA concentration, although 5-HT con¬ centrations in the MBH and POA were unaffected by GH administration. Exogenous GH has also been found to suppress 5-HT turnover in the rat dience¬ phalon (Stern et al 1975) and hypothalamus (Savard et al 1984) and to down-regulate 5-HT receptors (Popova et al 1991) but to elevate 5-HT and 5-HIAA concentrations in other brain areas (Stern et al 1975;Savard et al 1984). Since these changes in hypothal¬ amic 5-HT might be expected to increase the GH-releasing activity of the rat hypothalamus (Richardson et al 1981;Peterfreund & Vale, 1983), GH-induced changes in hypothalamic 5-HT metabo¬ lism may not simply correlate with GH autoregulation.…”

Section: Discussionmentioning

confidence: 96%

Growth hormone (GH) suppression of catecholamine turnover in the chicken hypothalamus: implications for GH autoregulation

Lea

Harvey²

1993

Journal of Endocrinology

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GH administered centrally or peripherally inhibits basal or secretagogue-induced GH secretion in domestic fowl. Since the release of pituitary GH is neurally regulated by the hypothalamus, GH autoregulation may be mediated by changes in the content or metabolism of hypothalamic monoamines. When chicken GH (500 micrograms/kg body weight) was injected i.v. into laying hens, tissue catecholamine (adrenaline, noradrenaline and dopamine) concentrations in the preoptic area (POA) and medial basal hypothalamus (MBH) were depleted for 2-24 h, as were concentrations of dihydroxyphenylacetic acid, a dopamine metabolite. The serotonin (5-HT) content of the POA and MBH was unaffected by i.v. GH administration, although a reduction in MBH 5-hydroxyindoleacetic acid suggested a tissue-specific inhibition of 5-HT turnover. Qualitatively similar results were observed in laying hens 24 h after the intracerebroventricular injection of chicken GH (10 micrograms/bird). These results therefore demonstrate aminergic actions of GH within the chicken hypothalamus which may mediate GH autoregulation. However, as amine metabolism is not only suppressed when endogenous GH secretion is reduced, but also at times when normal GH secretion is restored, these aminergic effects may also reflect other actions of GH on central function.

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“…These investigations led to the suggestion that TH is necessary for normal brain development in the fetus as it is during the early postnatal period (Obregon et al, 1984; Pérez‐Castillo et al, 1985). In other instance, the abnormal brain development observed during hypothyroidism, in rats, may partially result from a deficiency of GH (Savard et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…These investigations led to the suggestion that TH is necessary for normal brain development in the fetus as it is during the early postnatal period (Obregon et al, 1984;Pérez-Castillo et al, 1985). In other instance, the abnormal brain development observed during hypothyroidism, in rats, may partially result from a deficiency of GH (Savard et al, 1984). Oppenheimer and Schwartz (1997) and Ahmed et al (2008) reported that hyperthyroidism, during the brain development, results in cytoarchitecture abnormalities and disorganization of several neuronal cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II—The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system

Ahmed

El-Gareib

et al. 2012

Intl J of Devlp Neuroscience

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Excessive concentrations of free radicals in the developing brain may lead to neurons maldevelopment and neurons damage and death. Thyroid hormones (THs) states play an important role in affecting the modulation of oxidative stress and antioxidant defense system. Thus, the objective of this study was to clarify the effect of hypothyroidism and hyperthyroidism in rat dams on the neurons development of different brain regions of their offspring at several postnatal weeks in relation to changes in the oxidative stress and antioxidant defense system. The adult female rats were administered methimazole (MMI) in drinking water (0.02% w/v) from gestation day 1 to lactation day 21 to induce hypothyroidism and exogenous thyroxine (T4) in drinking water (0.002% w/v) beside intragastric incubation of 50--200 T4 μg/kg body weight (b. wt.) to induce hyperthyroidism. In normal female rats, the sera total thyroxine (TT4) and total triiodothyronine (TT3) levels were detectably increased at day 10 post-partum than those at day 10 of pregnancy. Free thyroxine (FT4), free triiodothyronine (FT3), thyrotropin (TSH) and growth hormone (GH) concentrations in normal offspring were elevated at first, second and third postnatal weeks in an age-dependent manner. In hypothyroid group, a marked depression was observed in sera of dam TT3 and TT4 as well as offspring FT3, FT4 and GH, while there was a significant increase in TSH level with the age progress. The reverse pattern to latter state was recorded in hyperthyroid group. Concomitantly, in control offspring, the rate of neuron development in both cerebellar and cerebral cortex was increased in its density and complexity with age progress. This development may depend, largely, on THs state. Both maternal hypothyroidism and hyperthyroidism caused severe growth retardation in neurons of these regions of their offspring from the first to third weeks. Additionally, in normal offspring, seven antioxidant enzymes, four non-enzymatic antioxidants and one oxidative stress marker (lipid peroxidation, LPO) followed a synchronized course of alterations in cerebrum, cerebellum and medulla oblongata. In both thyroid states, the oxidative damage has been demonstrated by the increased LPO and inhibition of enzymatic and non-enzymatic antioxidants in most examined ages and brain regions. These disturbances in the antioxidant defense system led to deterioration in the neuronal maturation and development. In conclusion, it can be suggested that the maldevelopment of neurons and dendrites in different brain regions of offspring of hypothyroid and hyperthyroid mother rat dams may be attributed, at least in part, to the excess oxidative stress and deteriorated antioxidant defense system in such conditions.

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Serotonin, 5-hydroxyindoleacetic acid and substance P content of discrete brain nuclei in rats made hypo- or hyperthyroid in the neonatal period: Effect of growth hormone treatment

Cited by 6 publications

References 34 publications

Thyroid hormones states and brain development interactions

Thyroid hormones states and brain development interactions

Growth hormone (GH) suppression of catecholamine turnover in the chicken hypothalamus: implications for GH autoregulation

Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II—The developmental pattern of neurons in relation to oxidative stress and antioxidant defense system

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