Development of Hypothalamic–pituitary–adrenal Response to Stress in Rats Made Hypothyroid by Exposure to Thiouracil From Conception

Meserve, Lee A.; Leathem, James H.

doi:10.1677/joe.0.0900403

Cited by 9 publications

(4 citation statements)

References 25 publications

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“…Thus, neonatal Tj administration re sults in an early increase in basal corticosterone titers and CBG levels [6,10,22] as well as in the early maturation of the adrenocortical response to stress [29]. In contrast, PTU administration during this period delays the maturation of the adrenocortical stress response and suppresses CRF-like activity in the hypothalamus [23,24]. These effects are con sistent with the effects on glucocorticoid receptor concen trations reported here.…”

Section: Discussionsupporting

confidence: 75%

Thyroid Hormones Influence the Development of Hippocampal Glucocorticoid Receptors in the Rat: A Mechanism for the Effects of Postnatal Handling on the Development of the Adrenocortical Stress Response

1987

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The role of thyroid hormones on the development of intracellular glucocorticoid receptor concentrations was examined in the hippocampus, hypothalamus, and pituitary of the rat. Adult animals, administered triiodothyronine (T3; 1.0 µg/g body weight) on days 1, 2, and 4 of life or thyroxine (T₄; 2.5 µg/g body weight) on days 1 and 2 of life, had significantly elevated glucocorticoid receptor concentrations in the hippocampus, but not in hypothalamus or pituitary. Adult animals treated with propylthiouracil (PTU; 0.2% in the mother’s food), a thyroid hormone synthesis inhibitor, for the first 2 weeks of life showed decreased glucocorticoid receptor concentrations in hippocampus, but not in hypothalamus or pituitary. We then examined whether thyroid hormones might mediate the effects of early stimulation on the development of hippocampal glucocorticoid receptor concentrations. Animals that were handled for 15 min daily (Ha) for the first 2 weeks of life showed increased hippocampal glucocorticoid receptor concentrations as adults compared to nonhandled (NHa) controls. PTU administration blocked the effects of handling, such that Ha/PTU animals showed hippocampal glucocorticoid receptor concentrations that were indistinguishable from those of NHa animals. In contrast, corticosterone administration over the first 2 weeks of life had no effect on adult hippocampal glucocorticoid receptor concentrations. These data suggest that thyroid hormones mediate, in part at least, the development of glucocorticoid receptor concentrations in the hippocampus and that this effect occurs independently of their effects on corticosterone titers.

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Section: Discussionsupporting

confidence: 75%

Thyroid Hormones Influence the Development of Hippocampal Glucocorticoid Receptors in the Rat: A Mechanism for the Effects of Postnatal Handling on the Development of the Adrenocortical Stress Response

1987

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“…We hypothesized that if 5-HT (or DA) did mediate central inhibition of ACTH release, then the hypothyroid model might show inhibition of ACTH/corticosterone response to stress. It has been previously shown that neonatal hypothyroid 1070 SMYTHE, BRADSHAW, AND VINING Endo • 1983 Volll3«No3 rats have reduced corticosterone responses to stress (29). However, in the present study, ACTH and corticosterone responses after either cold swim or ether stress in adult hypothyroid rats were comparable to the responses of normal adult rats.…”

Section: Discussioncontrasting

confidence: 62%

Hypothalamic Monoamine Control of Stress-Induced Adrenocorticotropin Release in the Rat*

1983

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Despite evidence that ACTH release after stress is under excitatory hypothalamic control, a stimulatory role for any of the monoamine neurotransmitters is yet to be clearly demonstrated. In the present investigation computerized gas chromatography/mass spectrometry was used to assess the neuronal activities of hypothalamic dopamine, norepinephrine (NE), and serotonin (5-HT) in rats after stress-induced ACTH release. Medial basal hypothalamic NE neuronal activity as assessed by the ratio of 3,4-dihydroxyphenylethyleneglycol (DHPG) to NE. (DHPG/NE) was elevated (P less than 0.0005) within 2 min after a 3-min cold water swim stress. Ether stress also caused a marked elevation in NE activity (P less than 0.0025). A highly significant positive correlation between the ratio of hypothalamic DHPG/NE and serum corticosterone was found over a large population of normal and stressed rats. Consistent with this relationship between hypothalamic NE neuronal activity and ACTH release being a causal one were the findings that 1) adrenalectomized rats exhibited markedly elevated hypothalamic DHPG/NE ratio and serum ACTH (both P less than 0.0005) together with serum corticosterone levels reduced to about 3% of control levels (P less than 0.0005), and 2) the administration to rats of the alpha-blocker yohimbine or the antianxiety agent diazepam resulted in significant changes in hypothalamic NE activity, together with parallel changes in ACTH secretion. In hypothyroid rats, which have elevated hypothalamic 5-HT activity, and in normal gentled rats, stress caused a significant reduction in hypothalamic 5-HT activity. High hypothalamic activity of dopamine or 5-HT in hypothyroid rats did not significantly affect basal ACTH levels nor prevent the responses to either cold water swim or ether stress, and both stresses resulted in elevated hypothalamic DHPG/NE, serum ACTH, and serum corticosterone (all P less than 0.005) in these animals. From these data it is concluded that NE is an excitatory hypothalamic monoamine for ACTH release in stress and that hypothalamic 5-HT activity is reduced after stress.

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“…Specifically, the developmental increase in this parameter was advanced approximately 3 days in hyperthyroid animals and was delayed approximately 3 days in hypothyroid animals. Previous studies on the effects of T4 status on the in vivo response of serum corticosterone to ACTH yielded conflicting results (22)(23)(24) and their interpretation was complicated by the use of a fluorometric assay which is known to be inappropriate in young rodents (1,…”

Section: Age (Days)mentioning

confidence: 99%

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

1986

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ABSTRACT. Infant rats exhibit a marked rise in serum concentrations of corticosterone between postnatal days 12 and 24. As this rise appears to be cued by L-thyroxine, the aim of the current study was to determine the physiological bases of the effects of both age and thyroid status on serum corticosterone. The in vivo response to either adrenocorticotropic hormone (60 mU/g body weight) or dibutyryl 3',5'-cyclic adenylate (0.3 mg/g body weight) increased between 10 and 16 days and was advanced and delayed by hyper-and hypothyroidism, respectively. In contrast, in vitro studies with adrenals from rats aged 10 and 16 days showed no effect of age on either basal or adrenocorticotropic hormone-stimulated production of corticosterone. Chronic administration of exogenous corticosterone to hyperthyroid animals resulted in significantly higher concentrations of serum corticosterone than did an identical administration to hypothyroid animals. In the neonatal rat, circulating concentrations of corticosterone are extremely low on days 6 through 12, then they rise markedly beginning on day 14 and reaching a peak on days 24-25 (1-3). During this same period the circulating concentrations of ACTH do not change significantly (4). Thus, either the ontogenic increase of corticosterone is independent of ACTH or the system becomes increasingly responsive to the basal concentration of ACTH. There is conflicting evidence regarding the latter possibility (4-6) and the data are difficult to interpret because of the use of a fluorometric method for measuring corticosterone which is now recognized to be inappropriate in young rodents (1, 2, 7).

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Development of Hypothalamic–pituitary–adrenal Response to Stress in Rats Made Hypothyroid by Exposure to Thiouracil From Conception

Cited by 9 publications

References 25 publications

Thyroid Hormones Influence the Development of Hippocampal Glucocorticoid Receptors in the Rat: A Mechanism for the Effects of Postnatal Handling on the Development of the Adrenocortical Stress Response

Thyroid Hormones Influence the Development of Hippocampal Glucocorticoid Receptors in the Rat: A Mechanism for the Effects of Postnatal Handling on the Development of the Adrenocortical Stress Response

Hypothalamic Monoamine Control of Stress-Induced Adrenocorticotropin Release in the Rat*

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

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