Dopaminergic Control of Thyrotropin, a-Subunit, Thyrotropin β-subunit, and Prolactin in Euthyroidism and Hypothyroidism: Dissociated Responses to Dopamine Receptor Blockade with Metoclopramide in Hypothyroid subjects*

Scanlon, M. F.; Chan, Vivian; Heath, Martha E.; Pourmand, M.; Rodríguez-Arnao, M. D.; Weightman, D.; Lewis, Meghan; Hall, R.

doi:10.1210/jcem-53-2-360

Cited by 51 publications

(19 citation statements)

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“…It has been shown recently that the effect of DA receptor blockade does not apply to TSH alone but affects also the a and p subunits [105] and that blockade of synthesis of do pamine with monoidotyrosine is as effective in elevating TSH levels as blockade of dopamine receptors [107]. It should be noted that the elevation of serum TSH levels fol lowing blockade of DA receptors is quite small and in nor mal subjects usually does not exceed 1.0 uU/ml.…”

Section: Dopaminementioning

confidence: 99%

“…Another factor is the thyroid status. Pa tients with primary hypothyroidism display a larger in crease than euthyroid controls [68,110], Within the hypo thyroid group the TSH response is inversely related to the severity of the condition [31, 105,110], Another determinant is possibly time of the day, because, according to Scanlon et al [108], the TSH release is more pronounced at the acrophase (around 23.00 h) of the human TSH daily rhythm than at its nadir (around 11.30 h). Finally, a greater reaction was observed in patients with hyperprolactinemia [69,95] which may reflect changes in metabolism of dopamine due to sustained elevation of prolactin levels.…”

Section: Dopaminementioning

confidence: 99%

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Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

Neuroendocrinology

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The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats. This is documented by observations that in humans, especially in subjects with primary hypothy-roidism, the dopamine precursor l-Dopa, dopamine receptor agonist bromocryptine, and dopamine itself decrease plasma levels of TSH and in some instances inhibit TSH secretory response to thyrotropin-releasing hormone (TRH). Conversely blockade of dopamine receptors leads to an elevation of circulating TSH. It is probable the dopaminergic drugs act on the pituitary thyrotrops rather than on the release of hypothalamic TRH. Analogous results were obtained in rats. In contrast, the noradrenergic system, studied mainly in rats, has a stimulatory influence on the secretion of TSH. This view is mainly supported by findings that acute interruption of noradrenergic neurotransmission causes a decrease of serum TSH levels and blocks the cold-induced stimulation of TSH secretion. The role of the central serotonergic system remains undecided because some experimental findings indicate that it has an inhibitory influence but others indicate an opposite function. The remaining transmitter systems have not been studied extensively enough to allow definite conclusions about their roles in the regulation of TSH secretion.

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Section: Dopaminementioning

confidence: 99%

Section: Dopaminementioning

confidence: 99%

Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

Neuroendocrinology

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“…Since the concentration of homovanilic acid is decreased in the cerebrospinal fluid in hyperthyroidism (17), the pro duction and turnover of dopamine by negative feedback may be decreased. Some investigators (18)(19) reported a diminished prolactin response to TRH in hyperthyroid ism, suggesting enhanced central dopaminergic tone.…”

Section: Introductionmentioning

confidence: 99%

Persistent Hemichorea Associated with Thyrotoxicosis.

et al. 1992

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We describe a case with unilateral chorea associated with thyrotoxicosis. A 23-year-old female with no family history of neurological diseases acutely developed choreic movements of the left extremities during gross thyrotoxicosis. CT scan and MRI study demonstrated no abnormality. Single-photon emission CT with technetium Tc 99m-labeled hexamethylpropyle neamine oxime revealed normal cerebral perfusion. Although the choreic movements were partially improved by dopamine antagonist, they persisted for two months until successful treatment of the thyrotoxicosis finally abolished these movements. Increased sensitivity of dopamine receptors may be responsible for persistent choreic movements in thyrotoxicosis.

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“…However, in the absence of concomitant gonadotropin fluctuations, a rise in «-sub levels in response to TRH [15,16] or antidopaminergic drug [17] administration, and a slight reduction after the infusion of pharmacological doses of DA [ 18] have been described also in normal subjects. Moreover, it is likely that «-sub responses to these specific agents depend upon thyrotroph stimulation, as they have been reported to be greater in primary hypothyroid patients [4,[17][18][19][20] and occur also in patients with hypogonadotropic hy pogonadism [16].…”

mentioning

confidence: 99%

“…Circulating TSH-|) derives only from thyrotroph secretion, but the low sensitivity of TSH-|1 RIA made difficull the assess ment of its responses to TRH, as well as to DA and antidopa minergic drug administration, except in hypothyroid patients [4,[17][18][19]21], However, the recent availability of a TSH-|i RIA with a sensitivity of 0.1 gg/l has allowed the detection of a slight increase in TSH-|) levels after TRH also in normal subjects [22].…”

mentioning

confidence: 99%

Thyrotropin Alpha- and Beta-Subunit Responses to Thyrotropin-Releasing Hormone and Domperidone in Normal Subjects and in Patients with Microprolactinomas

et al. 1991

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Microprolactinoma is a particular pathological situation characterized by the presence of increased hypothalamic dopaminergic tone reactive to tumoral hyperprolactinemia. Since dopamine (DA) is a physiological regulating factor of the secretion of thyroid-stimulating hormone (TSH), we investigated the responses of serum TSH (holo-TSH) and its subunits (α-subunit: α-sub, and TSH-β) to thyrotropin-releasing hormone (TRH) and domperidone (DOM; an antidopaminergic drug acting outside the blood-brain barrier) in 36 euthyroid subjects (20 controls and 16 patients with microprolactinoma) in order to evaluate the possible in vivo effects of DA excess on TSH subunit secretion. No significant difference in serum TSH increase after TRH (200 µg i.v.) was observed between patients with microprolactinoma and controls (TSH net incremental area under the curve, nAUC: 146 ± 9, mean ± SE, and 143 ± 7.7 µg/1/60 min, respectively), while serum α-sub and TSH-β responses were markedly reduced in patients with microprolactinoma as compared to those found in normals (α-sub nAUC: 3.0 ± 0.5 vs. 19.8 ± 2.2 µg/1/60 min, p < 0.001; TSH-β nAUC: 5.0 ± 0.8 vs. 9.5 ± 0.9 µg/1/60 min, p < 0.05). Serum TSH response to DOM administration (10 mg i.v.) was significantly higher in patients with microprolactinoma than in controls (TSH nAUC: 76 ± 12.7 vs. 28 ± 8.3 µg/1/90 min, p < 0.001), while serum α-sub increase was similar in the two groups (α-sub nAUC: 8.7 ± 4.8 and 10.2 ± 4.7 µg/1/90 min, p = NS), and serum TSH-β did not show any increase in patients with microprolactinoma (TSH-β nAUC: 0.2 ± 0.1 vs. 6.0 ± 3.3 µg/1/90 min, p < 0.001). The present findings show that in normal subjects, α-sub and TSH-β are cosecreted along with holo-TSH in response to both TRH and dopaminergic receptor blockade by DOM. On the contrary, in patients with microprolactinoma, α-sub and TSH-β responses to the above stimulatory agents are definitely impaired. Such an impairment is particularly evident after DOM administration which caused a holo-TSH release 3-fold higher than in controls. The discrepancy between the secretory response of holo-TSH and that of both α-sub and TSH-β in the condition of increased hypothalamic dopaminergic tone suggests a preferential secretion of holo-TSH molecules in order to overcome the chronic dopaminergic inhibition and maintain normal thyroid stimulation.

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Dopaminergic Control of Thyrotropin, a-Subunit, Thyrotropin β-subunit, and Prolactin in Euthyroidism and Hypothyroidism: Dissociated Responses to Dopamine Receptor Blockade with Metoclopramide in Hypothyroid subjects*

Cited by 51 publications

References 0 publications

Neurotransmitter Control of Thyrotropin Secretion

Neurotransmitter Control of Thyrotropin Secretion

Persistent Hemichorea Associated with Thyrotoxicosis.

Thyrotropin Alpha- and Beta-Subunit Responses to Thyrotropin-Releasing Hormone and Domperidone in Normal Subjects and in Patients with Microprolactinomas

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