Thyroid hormone regulation by stress and behavioral differences in adult male rats

Helmreich, Dana L.; Tylee, Daniel S.

doi:10.1016/j.yhbeh.2011.06.003

Cited by 78 publications

(59 citation statements)

References 60 publications

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“…Most research suggests that in rodents, circulating peripheral TH concentrations decrease in response to severe, uncontrollable stressors such as restraint stress or inescapable foot- or tailshocks (Langer et al, 1983, Bianco et al, 1987, Servatius et al, 2000, Helmreich et al, 2005, Helmreich et al, 2006, Helmreich and Tylee, 2011). These changes are likely due to a reduced secretion of these hormones by the thyroid gland (Helmreich and Tylee, 2011), but low T3 levels may also be the result of decreased activity of D1 in liver and kidney (Bianco et al, 1987).…”

Section: Gestational States and Conditions That May Alter Or Intermentioning

confidence: 99%

Influence of maternal thyroid hormones during gestation on fetal brain development

et al. 2017

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Thyroid hormones (TH) play an obligatory role in many fundamental processes underlying brain development and maturation. The developing embryo/fetus is dependent on maternal supply of TH. The fetal thyroid gland does not commence THs synthesis until mid gestation, and the adverse consequences of severe maternal TH deficiency on offspring neurodevelopment are well established. Recent evidence suggests that even more moderate forms of maternal thyroid dysfunction, particularly during early gestation, may have a long-lasting influence on child cognitive development and risk of neurodevelopmental disorders. Moreover, these observed alterations appear to be largely irreversible after birth. It is, therefore, important to gain a better understanding of the role of maternal thyroid dysfunction on offspring neurodevelopment in terms of the nature, magnitude, time-specificity, and context-specificity of its effects. With respect to the issue of context specificity, it is possible that maternal stress and stress-related biological processes during pregnancy may modulate maternal thyroid function. The possibility of an interaction between the thyroid and stress systems in the context of fetal brain development has, however, not been addressed to date. We begin this review with a brief overview of TH biology during pregnancy and a summary of the literature on its effect on the developing brain. Next, we consider and discuss whether and how processes related to maternal stress and stress biology may interact with and modify the effects of maternal thyroid function on offspring brain development. We synthesize several research areas and identify important knowledge gaps that may warrant further study. The scientific and public health relevance of this review relates to achieving a better understanding of the timing, mechanisms and contexts of thyroid programming of brain development, with implications for early identification of risk, primary prevention and intervention.

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Section: Gestational States and Conditions That May Alter Or Intermentioning

confidence: 99%

Influence of maternal thyroid hormones during gestation on fetal brain development

et al. 2017

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“…Activation of the HPA axis is associated with reductions in the release of thyroid stimulating hormone (TSH) and inhibition of conversion of thyroid hormone to biologically active forms (Charmandari et al, 2005). Deiodinase enzymes located within target tissues convert thyroxine (T4) to triiodothryonine (T3), the biologically active form of thyroid hormone or reverse T3 (rT3; Helmreich and Tylee, 2011), which binds to the thyroid receptor without activation. Thyroid hormones help regulate metabolic rate by altering expression of membrane ion pumps and can increase glucose oxidation rates in some species (Atkinson et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Thyroid hormones can increase the metabolic clearance of cortisol (Thompson, 2007), as well as inducing the release of cortisol at inflammation sites (Zoeller et al, 2007). Under conditions of chronic stress, cortisol promotes the expression of deiodonase enzymes that produce rT3 from T4 (Helmreich and Tylee, 2011).…”

Section: Introductionmentioning

confidence: 99%

Variation in adrenal and thyroid hormones with life-history stage in juvenile northern elephant seals (Mirounga angustirostris)

Jelincic

Tift

Houser

et al. 2017

General and Comparative Endocrinology

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“…T4) but may or may not impact other thyroid-related parameters. Strong agonists or antagonists would also be anticipated to influence clinical and behavioral observations (Fliers et al 2006;Helmreich & Tylee 2011). Stress may also impact the HPT axis (ibid); so, caution should be taken when evaluating findings in the presence of other systemic toxicity or when manipulating animals for thyroid hormone collection.…”

Section: Woe Evaluation For Potential Effects Of 24-d On the Hpt Axismentioning

confidence: 99%

Weight-of-the-evidence evaluation of 2,4-D potential for interactions with the estrogen, androgen and thyroid pathways and steroidogenesis

Neal

Marty

Coady

et al. 2017

Critical Reviews in Toxicology

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A comprehensive weight-of-the-evidence evaluation of 2,4-dichlorophenoxyacetic acid (2,4-D) was conducted for potential interactions with the estrogen, androgen and thyroid pathways and with steroidogenesis. This assessment was based on an extensive database of high quality in vitro, in vivo ecotoxicological and in vivo mammalian toxicological studies. Epidemiological studies were also considered. Toxicokinetic data provided the basis for determining rational cutoffs above which exposures were considered irrelevant to humans based on exceeding thresholds for saturation of renal clearance (TSRC); extensive human exposure and biomonitoring data support that these boundaries far exceed human exposures and provide ample margins of exposure. 2,4-D showed no evidence of interacting with the estrogen or androgen pathways. 2,4-D interacts with the thyroid axis in rats through displacement of thyroxine from plasma binding sites only at high doses exceeding the TSRC in mammals. 2,4-D effects on steroidogenesis parameters are likely related to high-dose specific systemic toxicity at doses exceeding the TSRC and are not likely to be endocrine mediated. No studies, including high quality studies in the published literature, predict significant endocrine-related toxicity or functional decrements in any species at environmentally relevant concentrations, or, in mammals, at doses below the TSRC that are relevant for human hazard and risk assessment. Overall, there is no basis for concern regarding potential interactions of 2,4-D with endocrine pathways or axes (estrogen, androgen, steroidogenesis or thyroid), and thus 2,4-D is unlikely to pose a threat from endocrine disruption to wildlife or humans under conditions of real-world exposures.ARTICLE HISTORY

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Thyroid hormone regulation by stress and behavioral differences in adult male rats

Cited by 78 publications

References 60 publications

Influence of maternal thyroid hormones during gestation on fetal brain development

Influence of maternal thyroid hormones during gestation on fetal brain development

Variation in adrenal and thyroid hormones with life-history stage in juvenile northern elephant seals (Mirounga angustirostris)

Weight-of-the-evidence evaluation of 2,4-D potential for interactions with the estrogen, androgen and thyroid pathways and steroidogenesis

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