Response of Hypothalamic Peptide mRNAs to Thyroidectomy

Ceccatelli, Sandra; Giardino, Luciana; Calzà, Laura

doi:10.1159/000126295

Cited by 53 publications

(24 citation statements)

References 43 publications

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“…Thereafter, prepro-TRH mRNA begins to rise (38), concurrent with TRH depletion in the median eminence and much of the hypothalamus (63). In thyroidectomized animals, prepro-TRH mRNA levels reach 155-190% of the euthyroid level by 14 days (38,42,63) and 200-250% of euthyroid control by 21 days or longer (11,12,34,38,53). These peak changes are comparable to those observed in this study, and the lack of accumulation of TRH transcripts in 16-day sleep-deprived animals may be consistent with the more gradual progression to a severely hypothyroxinemic state during sleep deprivation (8,23) than during experimental hypothyroidism.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation

Everson

Nowak

2002

American Journal of Physiology-Endocrinology and Metabolism

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Sleep deprivation in rats results in progressive declines in circulating concentrations of both total and free thyroxine (T4) and triiodothyronine (T3) without an expected increase in plasma thyroid-stimulating hormone (TSH). Administration of thyrotropin-releasing hormone (TRH) results in appropriate increases in plasma TSH, free T4, and free T3 across experimental days, suggesting deficient endogenous TRH production and/or release. This study examined transcriptional responses related to TRH regulation following sleep deprivation. In situ hybridization was used to detect and quantitate expression of mRNAs encoding prepro-TRH and 5′-deiodinase type II (5′-DII) in brain sections of six rats sleep deprived for 16–21 days, when there was marked hypothyroxinemia, and in sections from animals yoked to the experimental protocol as well as from sham controls. TRH transcript levels in the paraventricular nucleus (PVN) were essentially unchanged at 15–16 days but increased to about threefold control levels in three of four rats sleep deprived for 20–21 days, a change comparable to that typically found in prolonged experimental hypothyroidism. There was no evidence for suppression of 5′-DII mRNA levels, which would be a sign of T3 feedback downregulation of neurons in the PVN. A failure to increase serum TSH in response to hypothyroxinemia and to increased prepro-TRH mRNA expression indicates that alterations in posttranscriptional stages of TRH synthesis, processing, or release likely mediate the central hypothyroidism induced by sleep deprivation.

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Section: Discussionmentioning

confidence: 99%

Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation

Everson

Nowak

2002

American Journal of Physiology-Endocrinology and Metabolism

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“…102 Thyroid hormone also modulates glucose transport processes across the blood-brain barrier (BBB) 103 and in astrocytes, 104 and may alter the expression of glucose transporter one (GLUT-1) gene, the principal isoform responsible for glucose transport across the BBB. 105 Furthermore, the effects of thyroid hormones on CNS gene expression have been demonstrated for various other neuroactive peptides, eg, TRH, 106 corticotropin-releasing hormone (CRH), 107 brain-derived neurotrophic factor, nerve growth factor and neurotrophin 3, 108,109 angiotensinogen, 110 and several structural brain-specific genes (eg, myelin-associated glycoprotein, Pcp-2, microtubuleassociated proteins). 111 Of particular relevance is a recently reported interaction between thyroid and serotonin systems, indicating synergistic effects of T 3 and 5-HT 1A receptors on hippocampal brain-derived neurotrophic factor (BDNF) expression.…”

Section: Post-receptor and Molecular Actions Of Thyroid Hormonesmentioning

confidence: 99%

Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain

2002

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The use of thyroid hormones as an effective adjunct treatment for affective disorders has been studied over the past three decades and has been confirmed repeatedly. Interaction of the thyroid and monoamine neurotransmitter systems has been suggested as a potential underlying mechanism of action. While catecholamine and thyroid interrelationships have been reviewed in detail, the serotonin system has been relatively neglected. Thus, the goal of this article is to review the literature on the relationships between thyroid hormones and the brain serotonin (5-HT) system, limited to studies in adult humans and adult animals. In humans, neuroendocrine challenge studies in hypothyroid patients have shown a reduced 5-HT responsiveness that is reversible with thyroid replacement therapy. In adult animals with experimentally-induced hypothyroid states, increased 5-HT turnover in the brainstem is consistently reported while decreased cortical 5-HT concentrations and 5-HT 2A receptor density are less frequently observed. In the majority of studies, the effects of thyroid hormone administration in animals with experimentally-induced hypothyroid states include an increase in cortical 5-HT concentrations and a desensitization of autoinhibitory 5-HT 1A receptors in the raphe area, resulting in disinhibition of cortical and hippocampal 5-HT release. Furthermore, there is some indication that thyroid hormones may increase cortical 5-HT 2 receptor sensitivity. In conclusion, there is robust evidence, particularly from animal studies, that the thyroid economy has a modulating impact on the brain serotonin system. Thus it is postulated that one mechanism, among others, through which exogenous thyroid hormones may exert their modulatory effects in affective illness is via an increase in serotonergic neurotransmission, specifically by reducing the sensitivity of 5-HT 1A autoreceptors in the raphe area, and by increasing 5-HT 2 receptor sensitivity.

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“…Hypothyroidism is known to cause water retention and subsequent hyponatremia. Several reports suggest that this metabolic disorder is due to reversible derangement of renal tubular function [19,20], and not due to over-expression of ADH [21,22]. Therefore in this case, the supplementation of thyroxine may have contributed in part to normalizing the serum sodium concentration, but it may not be related to the suppression of ADH secretion.…”

Section: Cause Of Hypopituitarism Clinical Coursementioning

confidence: 78%

A Case of Initially Undiagnosed Hypoadrenalism Presenting Inappropriate Secretion of Anti-Diuretic Hormone.

1995

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Abstract.The case of a 55-year-old woman with inappropriate secretion of anti-diuretic hormone (ADH) is reported.Her pituitary-adrenocortical function test showed normal values on admission, but when she recovered from hyponatremia, severe panhypopituitarism became overt. Her adrenal insufficiency was considered to have been "masked" by endogenous stimulation of the hypothalamus-pituitaryadrenal axis under severe stress. One should be cautious in estimating the pituitary-adrenal function of severely ill patients.

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Response of Hypothalamic Peptide mRNAs to Thyroidectomy

Cited by 53 publications

References 43 publications

Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation

Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation

Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain

A Case of Initially Undiagnosed Hypoadrenalism Presenting Inappropriate Secretion of Anti-Diuretic Hormone.

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